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Case Study on Autism Severity Associated with Toxic Metals

Posted By Administration, Friday, October 1, 2010
Updated: Friday, April 18, 2014

Abstract 624138171_f262cd06cb_b

This study investigated the relationship of children's autism symptoms with their toxic metal body burden and red blood cell (RBC) glutathione levels. In children ages 3–8 years, the severity of autism was assessed using four tools: ADOS, PDD-BI, ATEC, and SAS. Toxic metal body burden was assessed by measuring urinary excretion of toxic metals, both before and after oral dimercaptosuccinic acid (DMSA). Multiple positive correlations were found between the severity of autism and the urinary excretion of toxic metals. Variations in the severity of autism measurements could be explained, in part, by regression analyses of urinary excretion of toxic metals before and after DMSA and the level of RBC glutathione (adjusted R2 of 0.22–0.45, P < .005 in all cases). This study demonstrates a significant positive association between the severity of autism and the relative body burden of toxic metals.


Autism is a severe developmental disorder which involves social withdrawal, communication deficits, and stereotypic/repetitive behaviour. The pathophysiological etiologies which precipitate autism symptoms remain elusive and controversial in many cases, but both genetic and environmental factors (and their interactions) have been implicated. One environmental factor that has received significant attention is the body burden of mercury, lead, and other toxic metals [1-5].
Bernard et al. [1] discussed the many similarities between the symptoms of children with autism and children poisoned by mercury. An epidemiology study by Windham et al. [2] found that the amount of airborne pollutants, and especially mercury, correlated with an increased risk for autism. A study by DeSoto and Hitlan [3] found that blood levels of mercury did significantly correlate with the diagnosis of autism. A small study by Adams et al. [4] found that children with autism had a 2-time higher level of mercury in their baby teeth than typical children. A study by Bradstreet et al. [5] investigated the body burden of toxic metals by giving dimercaptosuccinic acid (DMSA), an oral chelation medication approved by the FDA for treating infantile lead poisoning. They found that the children with autism excreted 3.1 times as much mercury into their urine (which is where DMSA is excreted), P < .0002, but lead and cadmium levels were not significantly different. Overall there is some evidence to suggest that mercury and possibly other toxic metals are related to the etiology of autism.
This study investigates the possible relationship of the severity of autism to the relative body burden of toxic metals. The severity of autism was assessed using four tools, a professional evaluation based on the Autism Diagnostic Observation Schedule [6], and parental evaluations based on the Pervasive Developmental Disorders Behaviour Inventory (PDD-BI) [7], the Autism Treatment Evaluation Checklist (ATEC) [8], and the Severity of Autism Scale (SAS). The individual burden of toxic metals was assessed based on urinary excretion, both before and after taking oral dimercaptosuccinic acid (DMSA). DMSA is a licensed medication for treating lead poisoning and indicated in cases meeting toxic criteria. DMSA is, however, widely used off-label for other metal exposures, for example, mercury. It acts by forming sulfhydryl linkages to divalent metal cations, forming a chelated metal complex which is then excreted in the urine [9]. Urine measurements before and after taking DMSA provide an indication of both ongoing environmental exposures (before DMSA provocation) and the accumulated or relative body burden (postprovocation with DMSA). Red blood cell (RBC) glutathione was measured because it is one of the body's primary means for excretion of toxic metals.
This paper investigates the possible relationship of the severity of autism to the body burden of toxic metals and RBC glutathione levels. This paper is part of a larger study which investigates the safety and efficacy of DMSA therapy, including both the biological consequences [10] and the DMSA associated behavioural effects [11]. The larger study involves a 3-day round of DMSA, to screen for admission into a 3-month DMSA treatment study; only children with high levels of urinary toxic metals were admitted into the long-term 3-month treatment study.

The methodology is discussed in detail in the companion paper [10]. Briefly, this study was conducted with the approval of the Human Subjects Institutional Review Board of Southwest College of Naturopathic Medicine. All parents and (where possible) children signed informed consent/assent forms. The study participants were recruited in Arizona, with the help of the Autism Society of America—Greater Phoenix Chapter and the Arizona Division of Developmental Disabilities.
The entry criteria were the following.
  • Children with autism spectrum disorder, diagnosed by a psychiatrist, psychologist, or developmental pediatrician.
  • Age 3–8 years.
  • No mercury amalgam dental fillings (due to a concern of their interaction with DMSA).
  • No previous use of DMSA or other prescription chelators.
  • No anemia or currently being treated for anemia due to low iron.
  • No known allergies to DMSA.
  • No liver or kidney disease.
  • Children are well hydrated (receiving adequate daily intake of water).
Four metrics were employed to assess the severity of autism: the PDD-BI, ATEC, SAS, and ADOS. Multiple assessment instruments were selected because they each provide insights into various aspects of autism. The ATEC was completed approximately 2-3 weeks prior to taking the DMSA, and the other three instruments were completed approximately 2–4 weeks after the initial 3-day round of DMSA, for children whose excretion of toxic metals was deemed high enough to warrant continuation in the long-term treatment study. The ATEC, PDD-BI, and SAS were assessed by the participant's parents, and the ADOS evaluation was performed by a certified ADOS evaluator. It should be noted that the ADOS was developed primarily for diagnosing autism, whereas the other tools were developed for assessing changes in autistic symptoms during treatment studies.
DMSA was administered orally in 9 doses of 10 mg/kg, 3 times daily, over 3 days. Urine was collected for approximately 8 hours prior to taking the DMSA, and for approximately 8 hours immediately after the 9th dose, in a process similar to a previous retrospective study of relative body burden of heavy metals [2]. RBC glutathione was measured approximately 1-2 weeks prior to taking the DMSA. The details of measuring the urinary metals and RBC glutathione are given in [10].
The PDD-BI is composed of many subscales. One of the subscales, the Semantic/Pragmatic Problems (SPPs), was difficult to interpret, since children with no spoken language inappropriately scored as less severely affected than those with limited language. Therefore, we exclude the SPP subscale in the Autism Composite score, resulting in a modified Autism Composite score consisting of Sensory/Perceptual Approach, Ritualisms/Resistance to Change, Social Pragmatic Problems, Social Approach Behaviors, Phonological and Semantic Pragmatic subscales. This modified Autism Composite score was discussed with I. Cohen, the developer of the PDD-BI. We believe that this modified subscale is more useful because several children initially without speech began talking after DMSA treatment in the study. The development of speech led to a worsening of their score on the SPP, because a nonverbal child is given a score of zero (indicating no semantic/pragmatic problems, which is the same score a typically developed child would receive) compared to a child with limited speech but major semantic/pragmatic problems who would receive a high score on the SPP. Thus, we think the modified Autism subscale (without the SPP) is more useful for children with very limited or no language.
In order to assess global changes in autism severity, a new metric was developed for this study. The Severity of Autism Scale (SAS) is introduced for the first time in this series of papers. It is essentially a Clinical Global Impression scale using a 0–10 severity scale, with the difference being that the scale was made specific to autism by defining the numeric values (see below). The purpose of the tool is to provide a simple, overall assessment of the severity of the symptoms of autism. In this study we will analyze the correlation of this scale with the other more established assessment tools.
Severity of Autism Scale:
  • 0: normal,
  • 1: slight symptoms of autism,
  • 2–4, mild symptoms of autism,
  • 5–7, moderate symptoms of autism,
  • 8–10, severe symptoms of autism.
63 participants were assessed with the ATEC, and 49 participants were assessed with the PDD-BI, SAS, and ADOS. Fewer participants were assessed for the latter three tests because some participants had low urinary excretion of toxic metals and were not eligible to continue, and some participants dropped out. Table 1 lists the characteristics of the participants.
Table 1
Characteristics of participants. The second number is the standard deviation.
Total participants 63
Male 57
Female 6
Age (years) 5.6 ± 1.6
Diagnosis 62 autism, 1 Asperger's

ATEC (total) 62 ± 28
SAS 5.1 ± 2.2
ADOS (communication + social) 15.8 ± 6.5
PDD-BI (modified autism score) −54.3 ± 62

RBC glutathione (pre-DMSA) 501 ± 246 micromolar
Table 2 lists their average urinary excretion of toxic metals before and after taking DMSA.
Table 2
Urinary excretion of toxic metals in Phase 1, at baseline and after 9th dose of DMSA, in mcg/g creatinine. Creatinine values have units of mg/dL. N = 63. The metals are listed in approximate order of effect of DMSA on excretion. Significant results are highlighted in bold font.
ElementBaselineAfter 9th doseAfter 9th dose versus baseline
Pb 1.3 ± 2.3 9.2 ± 7.8 638%****
Sn 2.3 ± 3.4 9.7 ± 24 314%**
Bi 0.18 ± 0.45 0.41 ± 1.0 128%**
U 0.015 ± .04 0.031 ± .1 111%
Hg 0.86 ± .92 0.97 ± 0.88 13%
Tl 0.15 ± 0.12 0.21 ± 0.19 42%***
Sb 0.10 ± 0.10 0.14 ± 0.20 42%*
W 0.3 ± 0.29 0.46 ± 0.50 18%**
Al 16 ± 21 19 ± 33 21%
Ni 6.7 ± 5.1 7.6 ± 4.3 12%
Cd 0.38 ± 0.24 0.3 ± 0.23 −14%
As 32 ± 20 25 ± 18 −19%**
Creatinine 94 ± 52 80 ± 43 −15%**
*P < .1, **P < .05, ***P < .01, ****P < .001

2.1. Regression Analysis
Regression analysis was employed to examine the relationship between the severity of autism (assessed by the ATEC, PDD-BI, SAS, and ADOS) and the urinary excretion of toxic metals, (both before and after taking DMSA), and further with the initial glutathione (in the red blood cells). For the selected dependent and independent variables, stepwise linear regression analyses were conducted: initially all independent variables were included in the regression; then at each step, the variable with the highest P-value was eliminated, and this process was continued until the adjusted Rvalue began declining. Thus, the goal was to determine the best fit to the sample data for the selected model, taking into account the correlation among the independent variables. Since the data had several missing values (due to missing lab or behavioural data), the regression analyses were conducted in two slightly different ways which generally yielded very similar results: ( 1) eliminate all participants with missing data for any of the variables in the model at the beginning of the analysis, and ( 2) eliminate participants on an as-needed basis (i.e., only where there is missing data for any variable in the current step in the analysis). Since these two methods yielded very similar results, for brevity we only report the results for method 1.
3.1. Correlations of Severity Scales
Table 3 shows the correlations among the assessment scales. There is a high correlation between the ATEC and the PDD-BI (r = 0.87), and a good correlation of the SAS with the ATEC (r = 0.70) and the PDD-BI (r = 0.72). The correlation of the ADOS with the other scales is somewhat lower (r
 = 0.60–0.67), probably since the ADOS evaluation was done by a professional evaluator, whereas the other assessments were done by the same parent.
Table 3
Correlation of autism severity scores.
 ATEC totalSASADOS (social + communication)PDD-BI (modified autism score)
ATEC 1      
SAS 0.70 1    
ADOS 0.60 0.60 1  
PDD-BI 0.87 0.72 0.67 1
3.2. Correlation Analysis
Table 4 shows the results of a simple correlation analysis of severity of autism versus toxic metal levels. Correlations with a P-value of less than .05 are shown in bold. Baseline excretion of antimony (Sb) and excretion of lead (Pb) after the 9th dose of DMSA are the two most consistent factors, although other metals also haveP < .05 for some of the severity scales. In all cases for P < .05, the correlations are positive, so that high levels of toxic metals correlate with higher severity of autism, as expected. Also, the initial glutathione correlates positively with two of the severity scales at P
 < .05.
Table 4
Correlation analyses of initial autism severity versus urinary metal excretion and initial glutathione. The metal excretion is measured both at Baseline (before DMSA) and after the 9th dose of DMSA. The first number in each cell is the correlation coefficient (r) and the second number is the P-value. Correlation coefficients with P < .05 are in bold. The last 2 rows list the total number of positive and negative correlation coefficients, respectively.
 ATEC totalADOS (social + communication)SASPDD-BI (modified autism score)
PbBase −0.00 (0.96) 0.11 (0.47) 0.50 (0.0002) 0.22 (0.12)
SnBase 0.16 (0.32) −0.11 (0.47) 0.12 (0.41) 0.09 (0.52)
TlBase 0.13 (0.32) 0.10 (0.49) 0.21 (0.15) 0.25 (0.077)
HgBase 0.13 (0.33) 0.05 (0.76) 0.15 (0.31) 0.18 (0.19)
SbBase 0.40 (0.002) 0.35 (0.02) 0.51 (0.0002) 0.42 (0.0023)
Wbase 0.16 (0.23) 0.07 (0.67) 0.26 (0.07) 0.17 (0.22)
AsBase 0.04 (0.74) −0.05 (0.73) 0.00 (0.98) 0.04 (0.76)
CdBase 0.00 (1.00) 0.11 (0.48) 0.03 (0.83) −0.10 (0.48)
AlBase −0.06 (0.65) −0.19 (0.20) −0.05 (0.73) 0.02 (0.87)
Pb9 0.27 (0.04) 0.34 (0.02) 0.36 (0.01) 0.42 (0.0027)
Sn9 −0.02 (0.88) 0.00 (0.98) 0.02 (0.87) −0.12 (0.42)
Tl9 0.26 (0.046) 0.11 (0.51) 0.27 (0.064) 0.24 (0.098)
Hg9 0.09 (0.52) 0.20 (0.18) −0.02 (0.91) 0.07 (0.59)
Sb9 0.03 (0.84) 0.20 (0.19) 0.38 (0.008) 0.26 (0.065)
W9 0.11 (0.42) 0.34 (0.02) −0.00 (0.99) 0.19 (0.18)
As9 0.19 (0.16) −0.24 (0.12) −0.24 (0.11) −0.04 (0.79)
Cd9 0.07 (0.58) 0.34 (0.024) 0.08 (0.57) 0.15 (0.29)
Al9 0.06 (0.65) 0.28 (0.059) 0.25 (0.089) 0.17 (0.24)
Glut1 0.25 (0.04) 0.34 (0.024) 0.25 (0.09) 0.26 (0.70)
Number of positive coefficients 17 15 15 16
Number of negative coefficients 2 4 4 3
However, because we are analyzing many correlations, a traditional 
P-value of < .05 is not a rigorous guide. Since we are analyzing 76 possible correlations, random chance alone would result in approximately 4 results at P < .05. We found 13 instances of P < .05 for toxic metals, and the probability of that occurring randomly is 7 × 10−5, so it is very likely that most, but probably not all, of the correlations represent actual relationships.
One way to deal with the problem of multiple correlation analyses is the Bonferroni approach. Using this approach involves dividing the nominal P-value by the number of tests, so that for 95% confidence one needs a P-value less than .05/76, or P < .0007. Using the Bonferroni approach, the correlations between initial Severity of Autism Scale (SAS) and baseline excretion of lead (Pb) and antimony (Sb) are significantly different from 0 at the 95% confidence level, and these are the only pairs that meet the Bonferroni criterion for the 5% significance threshold. Again, it should be noted that this is a conservative approach, designed to ensure that very few nonsignificant correlations are misrepresented as significant.
False discovery rate (FDR) is a less conservative method for performing multiple hypothesis tests, based on controlling the expected number of false positives among the cases declared significant. If we use FDR on the summary severity scores, then in addition to the results obtained from the Bonferroni analysis, the correlation between Initial ATEC Total and baseline excretion of antimony (Sb), and the correlations between Initial PDD-BI Autism Total and baseline excretion of antimony (Sb) and 9th dose excretion of lead (Pb) are significantly different from 0; we will term these findings “marginally significant.”
Next, consider the numbers of positive and negative sample correlation coefficients in the table. If there were no statistically significant correlations between autism severity and biological measures then we would expect on average about equal numbers of positive and negative sample correlation coefficients. For the summary severity measures, we observed 63 positive sample correlation coefficients (r's) and 13 negative r's. This corresponds to a P-value of 3 × 10−9 for the hypothesis that there is no correlation between the severity measures and biological measures. Thus it is extremely likely that there is a high overall positive correlation between the severity measures as a group and the biological measures taken as a group.
Finally, the average of all of the 76 sample correlation coefficients is 0.14. If there were no statistically significant correlations between autism severity and the biological measures, the average of 76 sample correlation coefficients (each of which was taken form a sample of size 40 or more) would come from a distribution with mean 0 and standard deviation equal to 0.02. Under those conditions, the P-value for a mean correlation coefficient of 0.14 is less that 10−10, so again it is extremely likely that there is a high overall positive correlation between the severity measures as a group and the biological measures taken as a group.
Since multiple correlations were obtained, it was decided to conduct regression analyses, which are discussed in the next section. Basically, a regression analysis allows for the simultaneous consideration of multiple factors, such as how well certain combinations of different toxic metal excretions can predict values of a specific autism severity measure.
3.3. Regression Analyses of Initial Severity of Autism
Tale 5 shows the results of stepwise linear regression analyses for the various autism severity scales as a function of urinary excretion of toxic metals (at baseline and after the 9th dose of DMSA) and initial glutathione. All of the analyses found that the variations in the severity of autism could be partially explained by the urinary excretion of toxic metals and initial glutathione, with adjusted R2 values ranging from 0.22 to 0.45, and P-values all below .005. For the ADOS (which had the highest adjusted R2), the most significant variables were mercury (Hg) and antimony (Sb) at baseline and mercury and tungsten (W) at the 9th dose.
Table 5
Regression analyses of initial autism severity versus urinary metal excretion and initial glutathione. In the regression equation, the suffixes for the metals refer to the value at Baseline (B) and after the 9th ( 9) dose of DMSA in Phase 1.
 AdjustedR2P-valueEquationMost significant variables
ATEC 0.22 .003 24.1–6.17 HgB + 76.6 SbB + 0.593 Pb9 + 3.97 Hg9 + 0.27 As9 SbB**, Pb9*
SAS 0.36 .002 4.81 + 1.70 PbB + 4.87 TlB − 0.640 HgB + 5.48 SbB − 1.87 CdB − 0.0237 AlB − 0.114 Pb9 − 3.14 Tl9 + 6.07 Sb9 PbB**
ADOS (comm. + social) 0.45 .0003 13.19–4.29 HgB + 24.1 SbB − 3.67 WB − 0.0673 AlB + 2.75 Hg9 + 6.60 W9 − 0.0539 As9 + 0.0054 Glut HgB**, SbB*, Hg9*, W9*
PDD-BI (modified autism score) 0.25 .004 −131.8 + 70.4 WB − 0.789 Sn9 + 18.8 Hg9 + 255 Sb9 + 21.8 W9 Sb9**, WB*, Sn9*
**P < .01, *P < .05

Since the ADOS score had the highest adjusted R2 values, we also conducted a similar regression analysis on the subscales—(a) language and communication; (b) reciprocal social interaction; (c) play; (d) stereotyped behaviors and restricted interests (SBRIs). Those results are show in Table 6. The variation in all four of the ADOS subscales could also be partially explained by urinary excretion of toxic metals and RBC glutathione (adjusted R2 of 0.21–0.41, P < .02 in all cases). The ADOS Sociability and the ADOS Communication subscales had the highest adjustedR2 (0.41 and 0.37, resp.). For the ADOS Sociability subscale, the most significant variable was tungsten at the 9th dose, followed by tungsten, aluminum, and thallium at baseline and lead and thallium at the 9th dose. For the ADOS Communication subscale, the most significant variables were mercury (at baseline and 9th dose) and antimony (Sb) at baseline.

Table 6
Regression analyses of initial ados subscales versus urinary metal excretion and initial glutathione. In the regression equation, the suffixes for the metals refer to the value at Baseline (B) and after the 9th ( 9) dose of DMSA in Phase 1.
 AdjustedR2P-valueEquationMost significant variables
ADOS-Sociability 0.41 0.004 8.70 + 1.20 PbB + 0.217 SnB + 12.7 TlB − 1.64 HgB − 10.2 SbB − 2.61 CdB − 0.631 AlB − 0.186 Pb9 − 7.13 Tl9 + 6.27 Sb9 +6.15 W9 +3.62 Cd9 W9***, AlB**, TlB*, HgB*, Pb9*, Tl9*
ADOS-Commun. 0.37 0.0003 2.39–2.57 HgB + 23.1 SbB + 2.32 Hg9 + .0048 Glut HgB**, Hg9**, SbB**
ADOS-Play 0.24 0.004 1.20 + 0.540 PbB + 4.23 Sb9 + 0.0017 Glut PbB*
ADOS-SBRI 0.21 0.02 4.64–0.897 HgB − 2.63 CdB − 0.26 AlB + 0.050 Pb9 + 0.730 Hg9  
***P < .001, **P < .01, *P < .05


Since the toxic metal excretions exhibit considerable correlation amongst themselves [10], one should refrain from reading too much into the relationships between specific metals and severity of autism and instead should interpret the results as indicating a general relationship between autism severity and urinary excretion of toxic metals.


The different assessment tools were found to be highly correlated, which generally supports the validity of each of the assessment tools. The correlations were the highest between the modified PDD-BI and the ATEC, suggesting that those scales are very consistent. The ADOS had a lower correlation with the other scales; this at least partly due to different evaluator for the ADOS (assessed by a professional certified in the ADOS) versus the ATEC, modified PDD-BI, and SAS which were assessed by the same person (the parent who was the primary care giver).
The various correlation analyses found that overall there were multiple positive correlations between the severity of autism and the urinary excretion of some toxic metals (both before and after taking DMSA). Lead (after DMSA) and antimony (at baseline) had the most consistent effect, but other metals were also important. The existence of multiple positive correlations suggested that a regression analysis was appropriate.
The regression analysis found that the body burden of toxic metals (as assessed by urinary excretion before and after DMSA) was significantly related to the variations in the severity of autism, for each of the four scales. The metals of greatest influence were lead (Pb), antimony (Sb), mercury (Hg), tin (Sn), and aluminum (Al). Different metals are significant for the different scales, and this partial disagreement is probably due to two factors. First, the severity scales are not identical, having somewhat different questions and evaluating symptoms somewhat differently; as pointed out in Table 3, the correlations between the scales are good but not identical. Second, it should be noted that the high correlation between urinary excretion of many of the metals (see Adams et al. [10]) makes it difficult to separate the effect of one metal from another. This makes it improper to assign too much meaning to specific regression variables and their coefficients. Thus, it is probably best to not overinterpret the results in terms of a particular metal, but to instead interpret them as evidence of the general role of toxic metals in relation to the severity of autism. Since oxidative stress and thiol metabolic disturbances have both been described in the autism population [12, 13], it is likely that these play a role in both relative burden and susceptibility to heavy metals. And since heavy metal exposure generates oxidative stress and thiol depletion, the potential etiological role of metal cations in generating autism symptoms should be further studied. Similarly, prior depletion of thiols and increased oxidative stress makes it more likely the individual will accumulate metals.
It should also be noted that each severity scale assesses a somewhat different aspect of autism; for example, the ATEC has a major section on physical health, which is not assessed by the other scales. So, that may also explain why the different scales have somewhat different relationships with different metals.
The ADOS had the highest adjusted R2 value, suggesting that it is a very useful scale for assessing the severity of autism and for inclusion in correlation and regression analyses with biological factors. This may be due to the fact that, of the four tools we used, only the ADOS involves a trained professional making a quantitative assessment of many children, whereas the other tools are assessments by parents of only their child.
The strong correlation of the SAS with the other scales, and the high adjusted R2value (0.36), suggests that the SAS is a useful tool for simple assessment of the severity of autism.
We are aware of two other studies which found a relationship between the severity of autism and a biomarker related to heavy metal toxicity. One study by Geier et al. [14] found that elevations in urinary porphyrins (associated with mercury or lead and mercury toxicity) were significantly associated with Childhood Autism Rating (CARS) scores. A second paper to report a relationship of the severity of autism with a biomarker was a study which found a strong inverse relationship of the severity of autism with the amount of mercury in the baby hair of the subjects [15]. However, a replication study [16] did not reproduce that correlation with severity. So, while two studies [14, 15] do support a possible relationship of variations in the severity of autism with body burden of toxic metals, as was found in this paper, additional research is needed to confirm this finding.
This paper has focused on the possible relationship between toxic metals and the severity of autism. It has not included an examination of the source of those metals. Mercury, lead, and other toxic metals come from many sources. There has been particular interest in the possible relationship of autism and thimerosal (a mercury-based preservative once used in many childhood vaccines, but removed from most vaccines after 2003). However, this study was not designed to determine the sources of the toxic metals found in children with autism.
4.1. Limitations of this Study
The original study was designed primarily for evaluating the safety and efficacy of DMSA therapy. It was not primarily designed for investigating the relationship of the severity of autism to toxic metals, but that was an interesting outcome, so we felt it worthwhile to report it. Some limitations of the study design include the following.
  • The PDD-BI, SAS, and ADOS were assessed 2–4 weeks after the first round of DMSA, whereas the ATEC was assessed before. However, the strong correlation of the ATEC and PDD-BI suggests that this was a minor issue, and that the initial round of DMSA did not significantly affect the assessment.
  • The ATEC involved the largest number of participants (n = 63), whereas the other assessments involved somewhat smaller numbers (n = 49).


Overall, the correlation analysis found multiple significant correlations of severity of autism and the urinary excretion of toxic metals, such that a higher body burden of toxic metals was associated with more severe autistic symptoms. The results of the regression analyses (P < .005 in all cases) indicate that variations in the severity of autism may be partially explained in terms of toxic metal body burden. However, the finding of a relationship does not establish causality.


First and foremost, the authors thank the many autism families and their friends who volunteered as participants in this research study. They thank the Wallace Foundation and the Autism Research Institute for financial support of this study. They thank Nellie Foster of SCNM for help with blood draws. They thank Women's International Pharmacy for assistance with compounding the DMSA individually for each child. They thank Spectrum Chemicals for providing the DMSA. They thank Doctor's Data and Immunosciences for providing testing at reduced cost. They thank the Autism Society of America—Greater Phoenix Chapter and the Arizona Division of Developmental Disabilities for their help with advertising the study.


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14. Geier DA, Kern JK, Garver CR, et al. Biomarkers of environmental toxicity and susceptibility in autism. Journal of the Neurological Sciences. 2009;280(1-2):101–108. [PubMed]
15. Holmes AS, Blaxill MF, Haley BE. Reduced levels of mercury in first baby haircuts of autistic children. International Journal of Toxicology. 2003;22(4):277–285. [PubMed]
16. Adams JB, Romdalvik J, Levine KE, Hu L-W. Mercury in first-cut baby hair of children with autism versus typically-developing children. Toxicological and Environmental Chemistry. 2008;90(4):739–753.

Source: J Toxicol. 2009; 2009: 532640. Published online 2009 August 26. doi: 10.1155/2009/532640. The Severity of Autism Is Associated with Toxic Metal Body Burden and Red Blood Cell Glutathione Levels. J. B. Adams,1* M. Baral,2 E. Geis,3 J. Mitchell,1 J. Ingram,3 A. Hensley,3I. Zappia,3 S. Newmark,4 E. Gehn,3 R. A. Rubin,5 K. Mitchell,3 J. Bradstreet,2, 6 and J. M. El-Dahr7

1Division of Basic Medical Sciences, Southwest College of Naturopathic Medicine, Tempe, AZ 85282, USA
2Department of Pediatric Medicine, Southwest College of Naturopathic Medicine, Tempe, AZ 85282, USA
3Autism Research Institute, San Diego, CA 92116-2599, USA
4Center for Integrative Pediatric Medicine, Tucson, AZ 85711, USA
5Department of Mathematics, Whittier College, Whittier, CA 90601-4413, USA
6International Child Development Resource Center, Phoenix, AZ, USA
7Department of Pediatrics, Tulane University School of Medicine, New Orleans, LA 70112, USA


Tags:  autism  heavy metal  toxins 

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Endometriosis and Diet - The Role of Fats

Posted By Administration, Thursday, September 30, 2010
Updated: Friday, April 18, 2014

by Fiona McCulloch, ND 2339180861_ae94f7d9c3_o

A recent study completed at Harvard Medical School found that eating a diet high in trans fat was associated with a 48% higher risk of developing laparoscopically confirmed endometriosis. It was also found that there was a 22% reduction in endometriosis in the group of patients in the highest fifth of long-chain omega 3 fatty acid consumption.

This was a prospective study of participants in the famous Nurses Health Study which followed 116 607 female registered nurses ranging in age from 25 to 42. This study initially found many correlations between infertility and nutrition.  Harvard researchers recently looked at the relationship specifically between fat consumption and the risk of developing endometriosis over 12 years for the nurses who had participated in the study.

The study also found that this association was even worse for women suffering from infertility. In these women, the association between trans fat consumption and endometriosis rose to to 78%.

Another fatty acid which was significantly correlated to endometriosis risk through this research was palmitic acid. Palmitic acid is mostly found in animal products such as red meat and dairy products and oils such as palm oil.  It was also found that women in the highest fifth of animal product intake were also 20% more likely to have endometriosis than those in the lowest fifth of animal product intake.

Other saturated (myristic, stearic) and monounsaturated (oleic, palmitoleic) fatty acids were not correlated to endometriosis. Total fat intake was also not related to the development of endometriosis, which was strongly correlated to the type of fat ingested.

It was calculated that if a woman were to increase by 1% of her calories from long chain omega 3 fatty acids (such as might be found in a high quality and high potency fish oil supplement) rather than from monounsaturated, saturated or omega 6 fatty acids (typical fat from animal or vegetable sources), this would give her a 50% reduction in risk for endometriosis.

Beware of labels: although recently on grocery shelves we see many packages labeled “0 trans fats” , many of these products may still actually contain hidden trans fats that can accumulate.  By law, in Canada, products with less than 0.2 grams trans fat per serving are allowed to be labeled free of trans fat and will be listed on the nutrition panel as having a total trans fat content of zero.  In the USA products that contain less than 0.5 grams trans fat per serving can be labeled free of trans fat.  This actually can allow a significant amount of trans fat to accumulate in the diet, unknown  and in some cases misleadingly to the consumer, so read labels carefully.  Even a couple of accumulated grams of trans fat per day can cause risks for health.  For endometriosis or other inflammatory diseases,  keep total trans fats to less than 1% of total calories per day (around 2 grams or less for an average woman) and increase long chain omega 3 fatty acids such as DHA and EPA found in high quality fish oil.

What to beware of:

  • Products labeled 0 trans fat, but which contain partially hydrogenated vegetable oil.  All partially hydrogenated oils contain trans fat.  Most trans fat free margarines do indeed contain trans fat, just in a smaller amount.
  • Palm oil, or palmitic acid.  This is often substituted in “trans fat free” products, and has been found to have many of the same detrimental health effects as trans fat.  Palmitic acid intake was found in this study to be corrleated to endometriosis, and is also correlated to other health risks such as cardiovascular disease
  • Excessive animal products.  These naturally contain 2-5% trans fat.


Stacey A. Missmer, Jorge E. Chavarro, Susan Malspeis, Elizabeth R. Bertone-Johnson, Mark D. Hornstein, Donna Spiegelman, Robert L. Barbieri, Walter C. Willett, and Susan E. Hankinson.  A prospective study of dietary fat consumption and endometriosis risk .  Hum. Reprod. 2010 25: 1528-1535.

Government of Canada.  Trans Fat monitoring program 2006.

FDA Guidance for Industry: Trans Fatty Acids in Nutrition Labeling, Nutrient Content Claims, Health Claims; Small Entity Compliance GuideAugust 2003

Tags:  diet  endometriosis  food and drink 

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Naturopathic Medicine Can Head Off Dementia

Posted By Administration, Wednesday, September 29, 2010
Updated: Friday, April 18, 2014

by Gina Nick, NMD, PhD 4353787172_ab791521eb_b (1)

A new study has determined the individual percentages by which a variety of lifestyle changes can reduce the risk of dementia and suggests that these interventions – in the absence of a new treatment for the mind-robbing disease – are likely to have the greatest impact on reducing dementia levels in the future. The study assessed previously identified risk factors such as depression, diet, alcohol consumption, educational level and vascular factors, which include heart disease, stroke, high blood pressure, obesity, diabetes, and high cholesterol. Results found that three changes together – eliminating depression and diabetes and increasing fruit and vegetable consumption – reduced dementia risk by a full 21 percent. Depression alone accounted for a 10 percent risk. Higher education was linked to an 18 percent lower risk. To illustrate the extent of these factors, the genetic tendency towards dementia accounts for seven percent of cases. The study was released August 5, 2010 and will be published in the British Medical Journal. But the journal already has made the full-text version of this important study available to the public, online without the usual requirement of a journal subscription or access fee.

Naturopathic Medicine is an effective approach to preventing and reversing depression and type two diabetes. Paired with diet ad lifestyle recommendations that are based on your unique constitution, licensed Naturopathic Medical Doctors have the tools to prevent and halt the progression of Dementia, even in the face of genetic predisposition. That offers true hope to millions of people!  It is time for Naturopathic Medicine, practiced by licensed Naturopathic Medical Doctors, to enter the mainstream and offer simple, genuine solutions to our healthcare crisis worldwide.

Tags:  dementia  naturopathic  prevention 

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Holistic Approach to Chronic Infections

Posted By Administration, Friday, September 24, 2010
Updated: Friday, April 18, 2014

by Gina Nick, NMD, PhD 4353787172_ab791521eb_b (1)

A new study has determined the individual percentages by which a variety of lifestyle changes can reduce the risk of dementia and suggests that these interventions – in the absence of a new treatment for the mind-robbing disease – are likely to have the greatest impact on reducing dementia levels in the future. The study assessed previously identified risk factors such as depression, diet, alcohol consumption, educational level and vascular factors, which include heart disease, stroke, high blood pressure, obesity, diabetes, and high cholesterol. Results found that three changes together – eliminating depression and diabetes and increasing fruit and vegetable consumption – reduced dementia risk by a full 21 percent. Depression alone accounted for a 10 percent risk. Higher education was linked to an 18 percent lower risk. To illustrate the extent of these factors, the genetic tendency towards dementia accounts for seven percent of cases. The study was released August 5, 2010 and will be published in the British Medical Journal. But the journal already has made the full-text version of this important study available to the public, online without the usual requirement of a journal subscription or access fee.

Naturopathic Medicine is an effective approach to preventing and reversing depression and type two diabetes. Paired with diet ad lifestyle recommendations that are based on your unique constitution, licensed Naturopathic Medical Doctors have the tools to prevent and halt the progression of Dementia, even in the face of genetic predisposition. That offers true hope to millions of people!  It is time for Naturopathic Medicine, practiced by licensed Naturopathic Medical Doctors, to enter the mainstream and offer simple, genuine solutions to our healthcare crisis worldwide.

Tags:  chronic  holistic medicine  infection 

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Plastics: The Sixth Food Group

Posted By Administration, Friday, September 17, 2010
Updated: Friday, April 18, 2014

by Ali Meschi, PhD, CNC

392577074_58467553b4_bPlastics, plastics, plastics everywhere.  Since the chemical dawn (Green Revolution) in World War I era the plastics have been everywhere, and we are just beginning to comprehend how chemicals in plastic affect and interfere with our health. Some of these chemicals are:

Phthalates are synthetic chemicals commonly found in food wraps, inks, adhesives, and vinyl floor coverings, some paints and of course most plastics used in daily life. Phthalates are plasticizers used to make plastic products more flexible. Their effects on human health are increasingly coming into question of alternative health care providers and the public. The offspring of female rats exposed to phthalates demonstrated a variety of abnormalities. “Most striking were their effects as androgen (male hormone) blockers in male offspring, which included a reduction of testosterone levels and abnormalities in a male productive tract.” A higher risk of miscarriage was observed among women exposed to high levels of phthalates.

The effects of hormone disrupting chemicals that leach out of plastic products has been the center of study at the University of Missouri for sometime. Bisphenol-A, an ingredient in the lining of metal food cans, polycarbonate water jugs, and dental sealants applied to children’s teeth, was found to alter the developments of male reproductive organs in mouse studies using amounts comparable to what humans currently ingest. Coating children’s teeth with Bisphenol-A to prevent dental cavities is being done by ever increasing numbers of dentists around the country, meanwhile researchers in Spain have found these substances can be an estrogen mimic compound which could cause cancer. Researchers at Tufts School of Medicine found saliva from Bisphenol-A treated patients to be estrogenic, however American Dental Association continues to defend the practice.

Man & Mouse
The Prostate glands of male mice were permanently enlarged, when their mothers were exposed to extreme dosage of Bisphenol-A (2 PPB). When doses reached to 20 parts per billion, daily sperm production was permanently decreased by 20%. This raises a valid question of relationship between human’s exposure to plastic chemicals and prostate problems, fertility problems, birth defects and cancer.

Would you like some Styrene with your coffee Mam?
Styrofoam cups and meat trays do more than just keeping your coffee hot and your meat neatly packaged. Nearly as pervasive as coffee break itself, white “plastic” or “foam” styrene cups outgas toxic chemicals into the coffee. As endocrine disrupters they are increasingly suspected of contributing to breast cancer, prostate cancer, thyroid and other glandular problems. One study of fat biopsies from human subjects conducted by the U.S. Environmental Protection Agency found styrene residues in 100 percent of the samples tested. Fat in humans and other mammals serves as a storage sites for many toxic chemicals which bioaccumulate over time, leaching out many years later, causing damage to cancer protecting genes. If more money were put into this area of cancer study instead of additional ways to use chemotherapy and radiation, we might make some headway in understanding cancer causation and prevention. Meat and cheese on styrene trays wrapped in clear plastic easily absorb lipid-loving chemicals from the packaging materials. Chemicals from styrene trays and some brands of plastic wrap easily migrate into foods with a high fat content. Removing foods from these packaging materials immediately after purchasing is strongly recommended. As a ritual it would be wise to substitute Styrofoam cups with washable ceramic mugs, this is both environmentally friendly and a good pro-health choice.


Plasticizers in plastic wrap migrate
Of seven brands tested by Consumer Reports, Reynolds Wrap and Saran Wrap contained some of the five plasticizers being tested. Studies indicate some plasticizers migrate into food at points of contact, even during refrigeration. Some cheese wrapped plastic was found to contain as high as 50 to 160 parts per million of the adipate plasticizer, DEHA. Waxed cheese with clear plastic overwrap found to have one to four parts per million of the common phthalate, DEHP. Consumers may wish to rewrap store bought cheese with waxed paper, or buy cheese cut to order at a deli and ask to have it wrapped in waxed paper.

Microwaveable plastics
Concerned consumers should avoid using plastic containers and plastic wrap in the microwave. Although manufacturers imply safety of the plastic container as “microwave safe”, the food safety when plastic is heated is a great concern. Dr. Carlos Sonnenschien of the Tufts University School of Medicine has been studying the chemical migration from plastics for over two decades. I strongly recommend substituting lead free glass or ceramic ware for microwave use. He became aware of this problem when studying blood samples that appeared to have been contaminated with a substance that caused an estrogenic effect in the blood cells. After tracking every possible source of contamination they concluded estrogen mimicking chemicals were leaching out of the new variety of plastic vials in which the blood was stored.

Is it “white- enamel” or is it simply plastic lined cans?
An increasing number of foods such as pumpkin, beets, chick peas and even chopped clams are packed in plastic lined cans, with no label information giving any clue. This can be shocking to find out that even some organic food producers such as Muir Glenn “organic” tomatoes are packed in plastic lined cans. A close inspection of the Muir Glen label revealed a sentence indicating the contents were “packed in lead-free white enamel-lined cans.” And not mentioning anything about Bisphenol-A on the label. An explanation of the difference between “white-enamel” and plastic lining did not offer any information from Muir Glen other than they are aware of the controversy surrounding the issue, and a statement from the National Food Processors Association’s position on Bisphenol-A: “most scientific authorities agree that there is no need for public health concern about cans lined with epoxy coating to help preserve their contents. Muir Glen which is now owned by General Mills, indicated that “enamel” was used “to avoid tinny taste.”

“Plastics, An important part of your healthy Diet”
An advertisement from the American P
lastics Council in National Geographic Magazine (2000), suggests that plastics could be thought of the as “the Sixth basic food group.”  “Oh, you certainly wouldn’t eat them, but plastic packaging does help protects our food in many ways,” assures the ad.

Maybe plastic does delay spoilage, however we are indeed eating plastic chemicals. Unknown to most consumers, many foods leach chemical from plastic packaging materials and plastic microwave containers. In addition, children are being exposed to chemicals from their plastic baby bottles, and teething rings to plastic toys. Perhaps plastic truly has become the sixth basic food group after all.

A flurry of studies show “the effects of Phthalates as an endocrine disrupter on the male reproductive system. Phthalates do their damage as anti-androgens, by blocking testosterone, and therefore inducing feminization symptoms in male lab rats.

Tags:  food and drink  plastic 

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The Specific Carbohydrate Diet

Posted By Administration, Wednesday, September 15, 2010
Updated: Friday, April 18, 2014

by Zina Kroner, DO 3375488854_0ed378b021_b  

Patients with inflammatory bowel disease (IBD) suffer from diarrhea and abdominal pain; this is often accompanied by difficulty in absorbing nutrients which results in weight loss. With ulcerative colitis, the large bowel (colon) is involved; Crohn’s disease can affect everything from the mouth to the anus, although usually small and/or large bowel disease usually predominates. Medical treatment of IBD is aimed at reducing the intestinal inflammation. 

Medications including sulfasalazine and related drugs and corticosteroids, taken orally or topically may be able to cause improvement in many patients. Stronger medications are frequently needed, with more side effects, including azathioprine, 6-mercaptopurine, methotrexate, and injectable anti-tumor necrosis antibody preparations. 

Surgery may be needed if medical treatment fails. In the case of ulcerative colitis, surgical procedures can be as drastic as removal of the entire colon with a permanent stoma (ostomy). Patients with Crohn’s disease may require surgery after surgery removing affected parts of the bowel.

For many patients, medical interventions are not enough, and surgery may be undesirable. There is another approach to treating IBD on a more basic level. This involves a significant change in diet for most people, to what is called the “Specific Carbohydrate Diet.” This diet can be undertaken along with any medical treatment.

This diet is available to anyone wanting to try it because of the late Elaine Gottschall (d. 2005). Gottschall was both a mother and a scientist who was able to find a way to help her own child, and decided to share her knowledge. In 1958, her eight-year-old daughter was suffering from ulcerative colitis that failed to respond to medical treatment. Looking for an alternative to surgery, Gottschall took her daughter to Dr. Sidney Haas, a 92-year-old physician who had published a textbook outlining his nutritional approach to healing the intestines. 

Dr. Haas quickly started the young girl on his specific carbohydrate diet. After a few months on the diet, her intestinal symptoms started to improve and she began to gain weight. After two years, she was well and free of symptoms of the disease. However, Dr. Haas had died in the interim and could no longer provide guidance.

Gottschall decided to learn more about the science behind the diet. She studied biology, cellular biology and nutritional biochemistry, earning a master’s degree and doing research on carbohydrate metabolism in the intestine. She published the Specific Carbohydrate Diet in a book first entitled Food and the Gut Reaction. It is now in its 13th printing, and called Breaking the Vicious Cycle: Intestinal Healing Through Diet. Over a million copies have been sold, and the book has been translated into seven other languages.

The Specific Carbohydrate Diet is based on the way carbohydrates are digested in the intestine, and what may be going wrong with the digestion in people with IBS and other intestinal disorders. Single sugars, including glucose, fructose and galactose can be transported from the intestine into the bloodstream without requiring digestion, in this case, splitting of molecules by enzymes. The cells of the small intestine must work harder to digest carbohydrates, as well as two-sugar molecules. 


Carbohydrates are broken down into disaccharides by salivary enzymes and pancreatic enzymes as they pass through the digestive tract. Disaccharides, comprised of two sugars, must be split into their component parts by enzymes located in the outer membrane of the cells in the small intestine. The cell membranes have small finger-like projections called microvilli that line the intestinal walls. The enzymes are located in the microvilli. There are four key disaccharide/enzyme pairs.

•Lactose, found in milk and milk products, must be broken down into glucose and galactose by the enzyme lactase.

•Sucrose, or table sugar, must be metabolized into glucose and fructose. Sucrose is fruit derived (cane sugar, beet sugar). As fruits ripen, sucrose can be broken down into glucose and fructose, so that ripe fruits may have less sucrose.

•Isomaltose is broken down into two molecules of glucose by isomaltase.

•Maltose is similarly metabolized into two glucose molecules by maltase.

A deficiency of any of these enzymes prevents the final digestion of disaccharides. They stay in the intestine where they can cause physical symptoms. For example, sugars can ferment and cause gas. 

Many people are affected by a lack of lactase, leading to the inability to fully digest the lactose in milk. This is called “lactose intolerance” which causes symptoms of gas, pain and diarrhea. The incidence of lactase deficiency varies between different ethnic groups, and is also more prevalent in older people than children. People with simple lactose intolerance can take a tablet containing lactase, or they can consume milk products which have lactase added. They can also usually tolerate milk products in which the lactose has been digested already. For example, in properly prepared yoghurt, the right kind of bacteria have already split and digested the lactose.

It has been postulated that in IBS, all of the disaccharidases are not functioning. Consequently, carbohydrate residues and disaccharides cannot be digested. These comprise so much of an average diet that the undigested material is a very significant amount. The symptoms of pain, gas and diarrhea are severe. 

The undigested disaccharides can feed the bacteria living in the intestine, causing an overgrowth of bacteria. Many kinds of bacteria normally live in the large intestine, and to a lesser degree, in the terminal ileum that connects to the large intestine. These can multiply and migrate up into the small intestine where they do not belong. 

Bacteria in the wrong place can cause damage to the lining of the small intestine, to the microvilli lining the small intestinal walls. This further reduces the amount of functional enzymes and perpetuates the cycle. Decreased digestion of carbohydrates and disaccharides allow bacteria to grow that damage the intestine and decrease the digestion of disaccharides even more. Additionally, the bacteria can release toxic byproducts that cause some of the symptoms of IBS.

Whatever begins the cycle of the intestinal damage, the decreased ability to digest carbohydrates and disaccharides leads to further damage, with more symptoms and even less digestive ability. The Specific Carbohydrate Diet interrupts the cycle.

The main principle of  the Specific Carbohydrate Diet is that only so-called “legal” carbohydrates are permitted. These are found in fruits, honey, properly-prepared yoghurt, and certain vegetables and nuts, and are to be used as follows:

•Fruits: Not introduced during the first one to two weeks. Then ripe, peeled and cooked. No raw fruits until diarrhea is under control. First raw fruit should be ripe mashed banana. No canned fruits with added sugar.

•Vegetables: No raw vegetables (such as salad greens and cucumbers)  until diarrhea is under control. Only frozen or fresh vegetables are allowed, not canned.

•Dairy products: No fluid milk. Specific cheeses are allowed. Homemade yoghurt is a large part of the diet. Dry curd cottage cheese is also important.

The following foods can also be eaten:

•Eggs: Added when diarrhea is less severe.


•Fats: Well tolerated in association with meat, butter, and allowed cheese and yoghurt.  Use of low-fat milk is not advised unless there is another reason.

Forbidden “illegal” carbohydrates:

•All cereal grains, including but not limited to corn, oats, wheat, rye, rice, millet, buckwheat, triticale or any other “new” grains such as quinoa. No products made from these grains are allowed, which means no bread, pasta, cakes, or other baked goods. Ground nut flours replace grains for baking. 

•No table sugar is allowed as a sweetener or in candy. It is sucrose, a disaccharide. Honey is the allowed sweetener. It contains glucose and fructose separately.

•No processed food, as starch (or disaccharides) are often added.

•No starchy vegetables, including potatoes and yams.

The diet should be as varied as possible. It is very difficult to follow the diet if you are a vegetarian, but not impossible. Consultation with a dietitian would probably be best if you want to follow the diet without any animal products. Anyone with a severe nut allergy will also have a very difficult time with the diet, since nut flour replaces all other carbohydrate flours.

Beginning the Diet

There are recipes in the SCD book, and specific foods you must buy and make before you can start the diet. There are suggestions for where to obtain needed products, and guidelines as to which brands are best. Beyond the information in the book, there are also cookbooks available as well as information on the SCD website. Whoever is going to prepare the food must be able to follow the recipes. In Gottschall’s words, the diet must be followed with “fanatical adherence” in order to work. Instructions on how to make the food for the beginning diet are on the website (

Sample menu for beginning the diet


  • Breakfast:

oDry curd cottage cheese (moisten with homemade yogurt)

oEggs (boiled, poached, or scrambled) – not if diarrhea is very severe

oPressed apple cider or grape juice mixed 1/2 and 1/2 with water. 

oHomemade gelatin made with juice, unflavored gelatin, and sweetener (honey)


  • Lunch: 

oHomemade chicken soup

oBroiled beef patty or broiled fish 

oHomemade Cheesecake


  • Dinner:

oVariations of the above

The above diet needs to be followed strictly. If you have a lot of diarrhea and cramping, you may need five days before you can add other foods. Some people only need a couple of days.

After diarrhea and cramps have stopped, you can add cooked fruit, ripe banana, and other vegetables, as well as egg if you did not start it earlier. You still need to avoid vegetables in the cabbage family. As you add a food, do it slowly, starting with a small portion and increasing it over a week.

Many people decide to try the diet for a month. Gottschall says that it usually takes three weeks to see an improvement, so if you feel absolutely no better after a month, you might want to reconsider whether or not you want to stay on the diet. Keeping a food journal may be the best way to document your symptoms and see if there is a trend toward improvement.

There is also a chance of a relapse of symptoms around the second or third month, which may occur because of a viral infection. Even if there is no specific cause, the symptoms will go away, so you should not be discouraged.

The Specific Carbohydrate Diet

The best way to collect all the information about the diet is from Gottschall’s book, other recommended cookbooks, recipes and tips, as well as places to buy the cookware and other items needed to make the foods, on the website (

You do not have to buy anything beyond the book if you are used to cooking and understand some of the more unusual foods you have to make, such as homemade yoghurt. There are no controls on portion or size in general. You can eat as much of “legal” foods as you want.

Here are some general instructions.

Allowable proteins

Essentially all fresh or frozen beef, lamb, pork, poultry, fish, eggs, specified cheeses, homemade yoghurt and dry curd cottage cheese, as well as fish canned in oil or water are allowed. No processed meats are allowed because they may contain filler carbohydrates (like in hot dogs) or they may have had added  sugars. No canned meats.

Allowable vegetables

Fresh or frozen, no canned vegetables or vegetables in jars. Dried peas and certain beans can be introduced after special preparation and when symptoms are better. No grains, no starchy root vegetables. Soybeans and soy products are not allowed

Allowable fruits

Fresh, raw or cooked, frozen or dried. Canned “in its own juice” with no added sugar is acceptable. Just about all fruits are allowed.

Allowable nuts

Just about all nuts in shells. Shelled nuts are acceptable if they have not been coated with starch when salted, which is usually the case with peanuts. 

Nuts should only be used as nut flour until diarrhea has stopped. Then they can be eaten whole.


Tomato juice is allowed, as is grapefruit juice, freshly squeezed. Orange juice should not be used in the morning when diarrhea is still active. If buying juice, avoid brands with added sugar. Many companies do not state this on the label. Bottled grape juice is usually without added sugar. Apple cider can be used, but not apple juice because sugar has been added. Juice boxes should be avoided.

You may also drink weak tea or coffee, and peppermint or spearmint herb tea. Other herb teas can worsen diarrhea. Only sweeteners allowed are honey or saccharin. Soft drinks with aspartame or NutraSweet may contain lactose and should be avoided. Instant coffee, tea and Postum are not permitted.

No liquid milk is allowed; no soy milk is allowed. 


You can use oils made from “illegal” foods for cooking, because the carbohydrates have been removed. Unflavored gelatin is used in dessert recipes. Sweets are allowed, made from honey, nuts and dates.

Some alcohol is allowed, including very dry wine, gin, Scotch, vodka and other similar. No cordials or liqueurs.

Once symptoms are under control and you are on the diet with all allowed foods, there is a great amount of variety allowed. There is generally no limit on portion sizes; you can eat as much as you want of allowed foods. There are sweets and treats, baked goods made with nut flour, substitutes suggested for pasta, and many clever ways to prepare food. 

Gottschall recommends that you stay on the diet for one year after your illness is  gone. She then suggests that you start “illegal” foods slowly, one at a time

While the diet is restrictive, it is balanced and able to provide a good source of most nutrients. Vitamin supplements are usually necessary, and you should discuss this with your physician. Many people begin this diet underweight because of their illness, and are able to gain weight. 

Does this diet work?

Thousands of people have used this diet successfully. Their stories have been documented on the website, in the form of testimonials as well as surveys.

One article was published in the journal Tennessee Medicine using data from the SCD site as well as follow-up conducted by two doctors. Two case studies were reported, one of a patient with Crohn’s disease and one patient with ulcerative colitis. Both were inadequately controlled on medication and had symptoms resolve on the diet. In these two cases, a physician reviewed colonoscopy reports and biopsies before and after the diet. In these two cases, the patients had demonstrable abnormalities which resolved.

In addition, survey material from the SCD website was used. 51 patients responded, 31 with Crohn’s disease and 20 with ulcerative colitis, Most of them were either in remission or much improved on the diet. Many of these individuals did not follow up with their physicians. 16 patients did have repeat colonoscopies, 12 of which were normal. This article ends with the following statement, “Proper randomized clinical trials are warranted to investigate the merits of this treatment (Nieves and Jackson, 2004).”

Large-scale randomized trials may never be done. Without a medication to study, there is no financial incentive to doing such a trial, and no source of funding. Many physicians will not accept treatments that have not been studied in such trials, and will not accept the Specific Carbohydrate Diet. However, other physicians will, and many patients have done very well on it. 

Should you decide to try the Specific Carbohydrate diet, you should actively discuss your progress with your doctor. As noted, you may need specific vitamins. You may also be able to lower medications, which you should do under a doctor’s care.


The  Specific Carbohydrate Diet website:

Breaking the Vicious Cycle: Intestinal Health Through Diet by Elaine Gloria Gottschall. Kirkton Press; Revised edition (August 1994). 13th printing, May 2010. (Available on, from Barnes and Noble, and elsewhere.)

Nieves R, Jackson RT. Specific Carbohydrate Diet in Treatment of Inflammatory Bowel Disease. Tennessee Medicine. 2004 Sep; 97(9):407. (This article can be viewed on the website). 

Tags:  diet  food and drink 

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The Mysery of Estrogen: The Good, the Bad, and Why It Has Gotten So Ugly!

Posted By Administration, Tuesday, September 7, 2010
Updated: Friday, April 18, 2014

by Holly Lucille, ND, RN  3823637057_8381a47751_b  

Is estrogen good? Is estrogen bad? Do I need it? These are just some of the questions I seem to be getting daily in my practice as the “story” about hormones gets increasingly confusing. Let’s take a deeper look at a not so simple category: estrogen!


Understanding Estrogens



Estrogen is among the most powerful class of hormones. Although we commonly think of estrogen as one substance or one type of hormone in our bodies, it is actually a class of naturally occurring sex hormones produced by the ovaries and the adrenal glands. There are at least two dozen known estrogens, all with various functions; every organ, including the brain, heart, ovaries, and liver, has estrogen-sensitive receptor sites. The most commonly discussed estrogens are estrone, estradiol, and estriol, produced in our bodies. But, estrogens produced in the body are not the only ones we are exposed to. Many women take estrogen replacement or supplementation and believe it or not, there are estrogens in the air we breathe, the water we drink, and the foods we eat.


Understanding the "Ugly" 

The main function of estrogens, as a group, is to tell cells to grow and proliferate. For example, they stimulate endometrial cells in preparation for pregnancy, prompt breast tissue growth, maintain function of the sexual organs, stimulate the menstrual cycle, and initiate the bodily changes that occur at puberty. If estrogen function and metabolism gets out of balance, cells can multiply unnecessarily, leading to dangerous situations, such as cancer in some cases.

Detrimental Estrogens 

We live awash in environmental “xenoestrogens”, foreign substances with estrogen like effects in the body, that negatively affect our health. They are absolutely everywhere!

It is important to note that their estrogenic activity is much more potent than the estrogen made by our bodies. Xenoestrogens can mimic natural estrogen or block it at estrogen receptor sites on cells throughout the body. These artificial estrogens activate receptors to stimulate a hormonal effect or occupy the receptor and block natural hormones from doing their job, either way disrupting normal endocrine activity. Many of these hormone imposters accumulate over time because they are fat soluble; they are easily absorbed through the skin and can be stored in body fat, where they can continue to interfere with the body’s natural hormone balance. These man-made estrogens find their way into the water supply, soil, air, and the food chain. As you might imagine, these have a serious effect on hormone balance. Most xenoestrogens are derived from petrochemicals and include pesticides, industrial chemicals, cleaners, plastics (water bottles, food containers), nail polish, and car exhaust. The pollution from these products causes health problems, including increased cancer rates and infertility.

Reducing Xenoestrogens in Your Life

Xenoestrogens are all around us—that’s a fact. Previously, their small amounts of estrogenic activity were dismissed, but recent findings published in Environmental Health Perspectives indicate all those little exposures add up. The researchers found that the effects of a collection of xenoestrogens, even though each one was beneath the levels at which they cause an effect, was to more than double the effect of natural estrogen by itself. How do you keep these minute exposures from making a difference in your health? Do what you can to minimize your exposure to xenoestrogens—you’ll find them in some unlikely places.


  • Avoid plastics for water and food storage. Use glass or ceramics whenever possible, especially to heat food. When plastic is heated, it rapidly diffuses into food. Use wax paper or a glass plate instead of plastic wrap to cover bowls in the microwave.
  • Use detergents with fewer chemicals. Chemical residue can be absorbed through your skin.
  • Choose shampoos, body soaps, makeup, and lotions that are paraben free.
  • Use natural pest control, not pesticides or herbicides.
  • Buy hormone-free meats; look for organics whenever possible.
  • Buy organic produce to reduce your exposure to herbicides, pesticides, and other chemicals.
  • Avoid birth control pills, spermicides, and HRT.

In a recent study published in the journal Occupational and Environmental Medicine, researchers made a direct link between cancer and pesticides. Women with breast cancer were five times more likely to have pesticide residue in their bloodstream than healthy women were. Synthetic hormones, in the form of birth control pills and HRT, introduce other man-made estrogens and provide another means of disrupting hormone balance, and as a result, health. These commercial hormones are structurally altered and different from the ones we produce. The list of risks related pills are at increased risk for high blood pressure and blood clots. Clotting can lead to sometimes-fatal strokes, heart attacks, or pulmonary emboli, depending on where the clot develops. Other serious adverse reactions, as listed in the Physicians’ Desk Reference (Medical Economics Co., 2003), include gallbladder disease and breast, liver, and endometrial cancer. Patients using oral contraceptives have reported numerous adverse reactions, including breast changes, colitis, congenital abnormalities, depression, impaired kidney function, menstrual changes, and weight changes.


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Natural Antibiotics

Posted By Administration, Thursday, September 2, 2010
Updated: Friday, April 18, 2014

by Joel Lopez, MD, CNS 2142814291_bfb2f412d1_o  

Are there such things? You bet! Ancient civilizations have used them in the past. Traditional medical systems such as Chinese medicine and Ayurvedic medicine texts are replete with information on natural germ fighting agents. 

In very recent times, just in 1987 in fact, one of the most comprehensive studies was conducted in Scotland that determined the most powerful antibacterial agents. These include the essential oils of thyme, cinnamon, clove and geranium. According to another study published in the International Journal of Food Microbiology, the oils of cinnamon, thyme and clove killed 92% of 25 different Gram negative and positive bacterial strains. As a side note, do you know that Listerine antiseptic was originally named after Joseph Lister, the Father of modern surgical antisepsis? The formula has the following essential oils, namely; thymol (from thyme essential oil), eucalyptol (from eucalyptus essential oil), methyl salicylate (from wintergreen essential oil) and menthol (from peppermint essential oil). A study done in 1999 published at the Journal of Clinical Periodontology showed that a mouthwash that had the essential oils of thyme, peppermint, wintergreen and eucalyptus, was more effective in improving oral health than an antiseptic that was fluoride-based. In 2006, powerful anti-fungal oils were identified by researchers and they include the following: essential oils of cinnamon, clove, lemongrass, geranium and thyme. They were all found to be equal or superior to a well-known anti-fungal medication. 

Other natural anti-fungal agents include garlic, caprylic acid (from coconut), melaleuca (tea tree oil) and Saccharomyces boullardii (an anti-fungal yeast). One common infectious cause of gastritis is H. pylori. Mastic gum has been used traditionally to treat this. Other agents were found to be effective in a study conducted at the Kyoto Prefectural University in Japan. These include the essential oils of manuka, cinnamon bark, carrot seed, savory, white grapefruit, clove and eucalyptus. Meanwhile, natural anti-viral agents include eugenol from clove oil (found to be effective against Herpes virus), peppermint oil, and manuka essential oil. Finally, what natural agents are effective against MRSA and VRE antibiotic-resistant bacteria? In studies done at the Western Infirmary in Glasgow, UK, it was found that melaleuca, lavender, peppermint and thyme essential oils showed the strongest activity against these germs. Anyway, I want to acknowledge Dr. Carolyn de Marco for providing a lot of great information regarding the use of essential oils. If someone is suffering from an infectious illness, work with your healthcare provider on how to improve your immune system so that you won’t get sick in the first place.

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Top Fertility Tests for Women: An Integrative Medicine Perspective

Posted By Administration, Monday, August 30, 2010
Updated: Friday, April 18, 2014

by Fiona McCulloch, ND

Top Fertility tests :  A Quick Reference for Women from an Integrative Medicine PerspectiveLab Testing for Infertility

FSH – Follicle Stimulating Hormone

Day 3 FSH can indicate how hard the pituitary is working to stimulate the ovaries.  Though traditionally a higher FSH is given a poor prognosis, I don’t always see it this way clinically.  The FSH can very much change depending on the quality of the antral follicles, which depends on ovarian health over the previous months as well as ovarian reserve.  The poorer the quality of the eggs, the more free radical damage they have accumulated and the poorer ovarian blood flow is, the more FSH the pituitary will have to put out in order to stimulate the antral follicles.  Healthy follicles are responsive to lower amounts of FSH.  If treatments are started to enhance ovarian health over 120 days of folliculogenesis prior to ovulation, the lowered FSH that can result can indeed indicate that the quality of the eggs in the ovaries has increased.  Please keep in mind that I have seen many women with high FSH become pregnant when egg quality and ovarian health is worked on so having a high FSH is not untreatable.

FSH Levels (Day 3)
Excellent less than 6 mIU/mL
Good 6-9 mIU/mL
Low 10-13 mIU/mL
Very Low above 13 mIU/mL

LH – Luteinizing Hormone

This is a test which is often done on day 3 of the cycle.  If higher than the FSH, especially if higher than a 2:1 ratio, it can indicate polycystic ovarian syndrome.  Having a high LH level will result in increased ovarian testosterone production,  altered estrogen production, and abnormalities with ovulation.  Normal day 3 range : <7 mIU/mL


Measured on day 3 of the cycle.  If elevated, estradiol can lower the fsh, thereby masking elevated fsh levels.  This can happen in cases of low ovarian reserve or functional cysts.  Estradiol can be low in conditions of low ovarian reserve.   Women who have estradiol over 294 pmol/L (or 80 pg/ml) have a lower chance of success with an IVF cycle since they will not respond to stimulation as well.


This is often measured on day 21.  This is used to determine whether ovulation has occurred as a healthy corpus luteum produces progesterone.  It is important to measure progesterone 7 days after your ovulation, measuring on day 21 only applies to women who ovulate on day 14.  Levels higher than 16 nmol/L strongly suggest an ovulatory cycle.


Often measured in the morning can indicate the impact of stress on the reproductive system.  Elevated cortisol can affect ovarian circulation and function.  Normal levels :  250 – 850 nmol/L taken between 6-8am.  Low cortisol can be found in congenital adrenal hyperplasia. Normal levels for am cortisol 101-536 nmol/L


The total level of testosterone in the system.  If elevated this can indicate polycystic ovarian syndrome.  High testosterone can interfere with normal ovulation often causing delayed ovulation or anovulation.   Levels can also be low around which can negatively affect ovarian function.  Normal levels for females 0.3- 4.0 nmol/L

Free testosterone

The amount of testosterone that is not bound to carriers and is available to stimulate tissues.  The higher this is, the more androgenic effect on the tissues.  This can be elevated in PCOS and specific adrenal conditions such as non-classical congenital adrenal hyperplasia (non classical CAH).  Normal levels for females 0.1-8.9 pmol/L


A hormone normally elevated in nursing and pregnancy.  If elevated in other situations it can interfere with ovulation and fertility.  It can be elevated due to stress, medications such as antidepressants or painkillers, thyroid disease, or pituitary conditions such as microadenomas.  normal levels in women 3.3 – 26.7 ug/l.

DHT – Dihydrotestosterone

A form of testosterone which is very potent.  DHT Can be elevated in pcos or enzyme conversion disorders resulting in androgen excess signs and symptoms.  Serum testing for DHT is often unreliable.

Sex hormone binding globulin
Can be low in patients with androgen excess conditions such as pcos or in hypothyroidism. Can be high in non classical CAH, hyperthyroidism.  Normal levels :  Follicular phase 24 – 200 nmol/L, Luteal phase 48 – 185 nmol/L


A long termarker of insulin resistance and blood glucose control. Can be elevated in pcos.  Marks the previous 3 months of blood glucose control.  Normal levels 0.040 – 0.060

A precursor to hormones, most especially androgens.  DHEA is made by the adrenal gland.  Levels tend to reduce with age and can be reduced in low ovarian reserve.  Levels can be elevated in PCOS.    Normal range for women 0-11 µmol/liter

A marker for stored iron.  Levels can be low in patients with infertility.   I recommend patients to achieve ferritin levels of above 50.

TSH -  thyroid stimulating hormone

I like to achieve levels of approximately 2 – 2.5.  Levels above this can put the patient at risk for early miscarriage.  Normal Ranges are :  0.4 – 4 mIU/L.   If levels are above 3, and especially if thyroid antibodies such as antithyroglobulin and anti-thyroid peroxidase are present with signs and symptoms of hypothyroidism, this and may present risks for fertility.

Vitamin D
Important for overall health, hormone balance, and stress levels.  Normal levels of 1, 25 Hydroxy Vitamin D 40 -150 pmol/L


A marker of inflammation and circulatory health.  This test is only recently being found to be important for ovarian health.  Elevated levels can be found in autoimmune conditions, ovarian aging and endometriosis.  Normal range : 4.7 – 14.1 umol/L

A measure of blood clotting.  Blood which clots excessively may interfere with implantation. Can also elevated in endometriosis or fibroids.  Normal value for INR 0.9 – 1.2

Anti sperm antibodies

The presence of anti- sperm antibodies in women can destroy or damage the sperm before they have the chance to fertilize the egg.  Around 5% of infertile women have these antibodies in their bloodstreams.
Anti thyroid antibodies

These include antithyroid peroxidase and antithyroglobulin.  These antibodies, if present will reduce fertility by 13%, even if thyroid function is normal.   These antibodies can cause alterations in thyroid function and also can be cross reactive with ovarian tissue.  Women with PCOS who don’t respond to clomid have a higher liklihood of having antithyroid antibodies.

Anti nuclear antibodies

These antibodies are present in autoimmune disease such as Lupus and Sjogrens syndrome.

Special Ovarian Reserve Markers:

Antimullerian hormone is produced by growing follicles and prevents premature recruitment of primordial follicles.  This value generally correlates with the number of functional primordial and antral follicles remaining in the ovary.  Generally, the higher the AMH,  the more healthy follicles are in the ovary.  Antimullerian hormone can predict the age of onset of menopause with some degree of accuracy.   Low AMH often does not give a good prognosis for IVF because IVF is based on the stimulation of multiple follicles – women with lower AMH tend to get fewer follicles during IVF stimulation.  However, even if AMH is low, conception is possible.  Even if there are not many follicles remaining in the ovary, their quality can be improved with treatments including antioxidants and circulatory enhancing therapies.  Natural conception with low AMH can and does happen.    Normal ranges :

AMH Levels
Optimal Fertility: 28.6 pmol/L – 48.5 pmol/L  or over 1.0 ng/ml
Satisfactory Fertility: 15.7 pmol/L – 28.6 pmol/L  or  over 1.0 ng/ml
Low Fertility: 2.2 pmol/L – 15.7 pmol/L or  0.3 – 0.9 ng/ml
Very Low/Undetectable: 0.0 pmol/L – 2.2 pmol/L or less than 0.3 ng/ml
High Level found in PCOS > 48.5 pmol/L or over 3 ng/ml

Inhibin b
A marker of ovarian function and reserve, this protein is secreted by small developing follicles and works to inhibit FSH levels, hence the name inhibin.  This test is completed on day 3 of the cycle.  As inhibin is secreted by the follicles, it can indicate the number of and function of the remaining folliciles. This test is not widely available.  Normal = above 45 pg/ml Low = below 45 pg/mL  Inhibin B is a spectrum however, and this line is a general guideline not a strict cutoff.  Like with AMH even if inhibin B is low, conception is possible if the health of the remaining follicles is enhanced.


Mosby’s Manual of Diagnostic and Laboratory Tests.  4th Ed. 2010

Speroff, Clinical Gynecologic Endocrinology and Infertility.  7th Edition 2005.

Tags:  fertility  Infertility 

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Vitamin C and Cancer Revisited

Posted By Administration, Friday, August 27, 2010
Updated: Friday, April 18, 2014

3237070041_a872337c89_oIn the issue of Proceedings of the National Academy of Sciences of the United States of America (PNAS), Chen et al. (1) it shows that i.p. injection of “pharmacologic doses” of vitamin C decreases the growth and weight of human, rat, and murine tumor xenografts in athymic, nude mice. This work follows a number of articles by the same group, led by Mark Levine at the National Institute of Diabetes and Digestive and Kidney Diseases, showing that millimolar concentrations of extracellular vitamin C kill cancer cells but not normal cells in a hydrogen peroxide (H2O2)-dependent manner (1–3). Such millimolar concentrations of vitamin C can be achieved in humans by i.v. infusion but not by diet or supplements (4). Hence, vitamin C is postulated to exert local pro-oxidant effects in the interstitial fluid surrounding tumor cells, killing them or inhibiting their growth, while leaving normal cells intact (1–3). 

It is well known that vitamin C, or ascorbic acid, is an effective biologic antioxidant and does not act as a pro-oxidant under normal conditions (5) because it does not readily autoxidize, i.e., react with oxygen (O2) to produce reactive oxygen species, such as superoxide radicals (O2•−) or H2O2. However, ascorbate readily donates an electron to redox-active transition metal ions, such as cupric (Cu2+) or ferric (Fe3+) ions, reducing them to cuprous (Cu+) and ferrous (Fe2+) ions, respectively (Reaction 1). In fact, reduction of copper or iron in the catalytic site of certain enzymes underlies ascorbate's well known biologic function as a co-substrate in procollagen, carnitine, and catecholamine biosynthesis (6). Reduced transition metal ions, in contrast to ascorbic acid, readily react with O2, reducing it to superoxide radicals (Reaction 2), which in turn dismutate to form H2O2 and O2 (Reaction 3): 

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The H2O2 produced this way (Reactions 1–3) seems to be key to ascorbate's antitumor effect because H2O2 causes cancer cells to undergo apoptosis, pyknosis, and necrosis (2). In contrast, normal cells are considerably less vulnerable to H2O2. The reason for the increased sensitivity of tumor cells to H2O2 is not clear but may be due to lower antioxidant defenses (7). In fact, a lower capacity to destroy H2O2—e.g., by catalase, peroxiredoxins, and GSH peroxidases—may cause tumor cells to grow and proliferate more rapidly than normal cells in response to low concentrations of H2O2. It is well known that H2O2 exerts dose-dependent effects on cell function, from growth stimulation at very low concentrations to growth arrest, apoptosis, and eventually necrosis as H2O2 concentrations increase (8). This dose-dependency may be shifted to the left in tumor cells, making them more sensitive to both the growth stimulatory and cytotoxic effects of H2O2. Whatever the exact mechanism, the increased sensitivity of tumor cells to killing by H2O2 may provide the specificity and “therapeutic window” for the antitumor effect of extracellular ascorbate (1, 2). 


Millimolar concentrations of extracellular vitamin C kill cancer cells but not normal cells. 

The chemical reactions linking ascorbate to H2O2, as explained above (Reactions 1–3), require a redox-active transition metal—without it, ascorbate cannot exert pro-oxidant effects. Chen et al. (2) speculate that there is an extracellular “metalloprotein catalyst” of between 10 and 30 kDa in size that interacts with ascorbate. Identification of this metal-containing protein will be critical because it seems to be the cause for millimolar concentrations of ascorbate to act as a pro-oxidant in interstitial fluid. In contrast, the protein must be absent or inactive in blood, otherwise ascorbate would become oxidized to the ascorbyl radical or be unstable, which is not observed (1). If this putative metalloprotein can be identified and characterized, it may serve as an additional target for anticancer therapy. For example, other naturally occurring reducing agents, such as certain flavonoids or thiol compounds, may be particularly effective in reducing the protein's metal center, or drugs may be developed specifically targeting this center. 

Although Chen et al. (1) provide no direct evidence for the existence of the metalloprotein or the formation of reduced transition metal ions by extracellular ascorbate, they measure the other reaction product formed between ascorbate and the putative metal center, i.e., the ascorbyl radical (Reaction 1). They show formation of this radical in a time-dependent and ascorbate-dose-dependent manner in interstitial fluid of tissues, including tumor xenografts, but not in blood (1, 3). They also show that the concentration of the ascorbyl radical correlates with the concentration of H2O2 in interstitial fluid, whereas no H2O2 can be detected in blood or plasma (3, 9). These observations, combined with the inhibitory effect on xenograft growth, provide the proof of concept that millimolar concentrations of extracellular ascorbate, achievable by i.p. injection or i.v. infusion in experimental animals and humans, respectively, exert pro-oxidant, antitumor effects in vivo


Why is it important to understand how vitamin C can produce H2O2 and kill cancer cells but not normal cells? Because without this detailed knowledge, we do not have a scientific rationale to revisit the question of whether i.v. infusion of vitamin C may have value in treating cancer patients. The potential cancer-therapeutic activity of vitamin C has a long and controversial history. In 1973, Linus Pauling and Ewan Cameron (10) postulated that vitamin C inhibits tumor growth by enhancing immune response and stabilizing glycosaminoglycans of the extracellular matrix by inhibiting hyaluronidase. Cameron and Campbell (11) reported on the response of 50 consecutive patients with advanced cancer to continuous i.v. infusions (5–45 g/d) and/or oral doses (5–20 g/d) of vitamin C. No or minimal response was observed in 27 patients; 19 patients exhibited tumor retardation, cytostasis, or regression; and 4 patients experienced tumor hemorrhage and necrosis. The first clinical study by Cameron and Pauling (12) compared survival times between 100 patients with terminal cancer treated with i.v. and oral vitamin C, usually 10 g/d, and 1,000 comparable patients not given vitamin C. Patients treated with vitamin C survived approximately four times longer than controls, with a high degree of statistical significance (P < 0.0001). A follow-up study reported that patients given vitamin C had a mean survival time almost 1 year longer than matched controls (13). Overall, 22% of vitamin C-treated patients but only 0.4% of controls survived for more than 1 year. 

The National Cancer Institute sponsored two randomized, placebo-controlled, double-blind trials of vitamin C and advanced cancer at the Mayo Clinic (14, 15). In both trials, patients were given 10 g/d vitamin C or placebo. Survival rates were essentially the same for all groups. Plasma concentrations of vitamin C were not measured in either study, and vitamin C was given only orally. In retrospect, the Mayo Clinic trials may have failed to properly evaluate the clinical efficacy of vitamin C in cancer because of insufficient plasma concentrations of vitamin C attained with oral supplementation (4). 

Pauling and colleagues (16) emphasized host resistance to cancer but recognized the anticancer role of redox chemistry, especially reactive oxygen species formed from the reaction of vitamin C with copper. When mice were inoculated with Ehrlich tumor cells and injected i.p. with the copper-containing tripeptide copper:glycylglycylhistidine (Cu:GGH) and vitamin C, 40% survived 60 days, whereas no controls survived for longer than 30 days. The combination of Cu:GGH and vitamin C was also toxic to Ehrlich tumor cells in vitro, but the cytotoxicity was abrogated by catalase, suggesting that H2O2 was the cytotoxic species. The work of Chen et al. (1–3) also strongly suggests that H2O2 is responsible for the anticancer activity of vitamin C. 

Interestingly, Chen et al. (1) noted that metastases were present in ≈30% of athymic mice grafted with glioblastoma tumors, whereas no metastases were detected in similar mice injected i.p. with ascorbate. This observation warrants further investigation because metastases account for a substantial percentage of cancer mortality.   


Two Phase 1 clinical trials of cancer and vitamin C have recently been published that demonstrated remarkable tolerance and safety for high-dose (up to 1.5 g/kg) i.v. vitamin C in patients screened to eliminate hyperoxaluria, glucose-6-phosphate dehydrogenase deficiency, and other medical conditions (17, 18). Additionally, a series of case reports indicated that high-dose i.v. vitamin C was associated with long-term tumor regression in three patients with advanced renal cell carcinoma, bladder carcinoma, or B-cell lymphoma (19). Clinical plausibility has been repeatedly suggested, and Chen et al. (1–3) now have convincingly demonstrated biologic plausibility and are poised to explore the potential value of “pharmacologic ascorbate in cancer treatment” in humans. 


The authors declare no conflict of interest. See companion article on page 11105. 


1. Chen Q, et al. Pharmacologic doses of ascorbate act as a prooxidant and decrease growth of aggressive tumor xenografts in mice. Proc Natl Acad Sci USA. 2008;105:11105–11109. [PMC free article] [PubMed] 

2. Chen Q, et al. Pharmacologic ascorbic acid concentrations selectively kill cancer cells: Action as a pro-drug to deliver hydrogen peroxide to tissues. Proc Natl Acad Sci USA. 2005;102:13604–13609. [PMC free article] [PubMed] 

3. Chen Q, et al. Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo. Proc Natl Acad Sci USA. 2007;104:8749–8754. [PMC free article] [PubMed] 

4. Padayatty SJ, et al. Vitamin C pharmacokinetics: Implications for oral and intravenous use. Ann Intern Med. 2004;140:533–537. [PubMed] 

5. Carr A, Frei B. Does vitamin C act as a pro-oxidant under physiological conditions? FASEB J. 1999;13:1007–1024. [PubMed] 

6. Englard S, Seifter S. The biochemical functions of ascorbic acid. Annu Rev Nutr. 1986;6:365–406. [PubMed] 

7. Oberley TD, Oberley LW. Antioxidant enzyme levels in cancer. Histol Histopathol. 1997;12:525–535. [PubMed] 

8. Davies KJ. The broad spectrum of responses to oxidants in proliferating cells: A new paradigm for oxidative stress. IUBMB Life. 1999;48:41–47. [PubMed] 

9. Frei B, Yamamoto Y, Niclas D, Ames BN. Evaluation of an isoluminol chemiluminescence assay for the detection of hydroperoxides in human blood plasma. Anal Biochem. 1988;175:120–130. [PubMed] 

10. Cameron E, Pauling L. Ascorbic acid and the glycosaminoglycans. Oncology. 1973;27:181–192. [PubMed] 

11. Cameron E, Campbell A. The orthomolecular treatment of cancer. II. Clinical trial of high-dose ascorbic acid supplements in advanced human cancer. Chem-Biol Interact. 1974;9:285–315. [PubMed] 

12. Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: Prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA. 1976;73:3685–3689. [PMC free article] [PubMed] 

13. Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: Reevaluation of prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA. 1978;75:4538–4542. [PMC free article] [PubMed] 

14. Creagan ET, et al. Failure of high-dose vitamin C (ascorbic acid) therapy to benefit patients with advanced cancer. A controlled trial. N Engl J Med. 1979;301:687–690. [PubMed] 

15. Moertel CG, et al. High-dose vitamin C versus placebo in the treatment of patients with advanced cancer who have had no prior chemotherapy: A randomized double-blind comparison. N Engl J Med. 1985;312:137–141. [PubMed] 

16. Kimoto E, Tanaka H, Gyotoku J, Morishige F, Pauling L. Enhancement of antitumor activity of ascorbate against Ehrlich ascites tumor cells by the copper:glycylglycylhistidine complex. Cancer Res. 1983;43:824–828. [PubMed] 

17. Riordan HD, et al. A pilot clinical study of continuous intravenous ascorbate in terminal cancer patients. PR Health Sci J. 2005;24:269–276. 

18. Hoffer LJ, et al. Phase I clinical trial of i.v. ascorbic acid in advanced malignancy. Ann Oncol. 2008 doi: 10.1093/annonc/mdn 377. [Cross Ref] 

19. Padayatty SJ, et al. Intravenously administered vitamin C as cancer therapy: Three cases. Can Med Assoc J. 2006;174:937–942. [PMC free article] [PubMed]

Source: Frei, Balz. Lawson, Stephen. Linus Pauling Institute, Oregon State University, Corvallis, OR 97331. Proc Natl Acad Sci U S A. 2008 August 12; 105(32): 11037–11038. Published online 2008 August 5. doi: 10.1073/pnas.0806433105. 

Tags:  cancer  vitamin C 

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Tumeric and Alzheimer's Disease

Posted By Administration, Monday, August 23, 2010
Updated: Friday, April 18, 2014

by Holly Lucille, ND, RN 1481271856_d1046f2f35_b  

In India, Alzheimer's disease is relatively uncommon. People over the age of 65 living in certain rural areas of India have a less than 1 percent (0.84%) chance of developing the disease. In the larger cities and rural areas of India, the risk is just 2.4 percent.(1,2)

Compare these findings to people over the age of 65 living in the United States. Again, depending on where we are living, our chances of developing Alzheimer's disease range from a little under 5 percent to an astonishing 17 percent.(3,4)

So what are people who are living in India doing that we aren't doing here in the US to account for these dramatic differences? The answer seems to be curry, that zesty spice and staple of Indian foods. Research has shown that a compound in curry not only prevents changes in the brain that lead to Alzheimer's disease, it actually reverses some of the damage already present.(5)

  • How can curry prevent these changes in the brain? Isn't that a lot to expect from a spice?
Evidently, it's not too much to expect from this spice. Curry comes from the turmeric plant - Curcuma longa is the plant's official name. Curcumin, a plant compound in turmeric, is the source of curry's instantly recognizable bright yellow pigment. When it comes to the scientific research of Curcuma longa, the terms curcumin and turmeric are both used. Both refer to the same thing - turmeric extract.(6)

There have been more than 1300 studies on turmeric and its health benefits for humans. Research has shown turmeric is able to help the body get rid of cancer-causing toxins. Turmeric also blocks estrogen receptors and enzymes that promote cancer. And it's been found to stop the growth of new blood vessels in cancerous tumors - an important factor in keeping cancer from getting larger and spreading throughout the body.(7-9)

But one of turmeric's most exciting health benefits is its ability to reduce, prevent, and stop inflammation. While inflammation is a normal and needed response to injury or disease, chronic inflammation can cause damage to tissues. And researchers are now finding inflammation plays a huge role in Alzheimer's disease.


  • I've always heard that Alzheimer's disease was caused by complex growths in the brain called plaques and tangles. How can simple inflammation cause such a devastating disease?

You are right. Plaques and tangles are indeed the hallmarks of Alzheimer's disease. But researchers looking at the brain damage caused by Alzheimer's have always noted the presence of inflammation wherever plaques and tangles form.(10) In the past, this inflammation was thought to be simply a consequence of Alzheimer's disease. Now scientists believe the inflammation itself starts a chain reaction ultimately contributing to the development of Alzheimer's disease.(11)

When cells in the brain are disrupted by inflammation, amyloid, a protein normally found in the brain, begins to act chaotically. This chaos results in the creation of beta-amyloid, a protein that is toxic to cells in the brain. Sticky deposits of beta-amyloid build up and collect around the cells, making dense clumps or plaques. Because the brain can't break the plaques down or get rid of them, they stay right where they are and slowly accumulate.(10,12,13)

Tangles result when long protein fibers that act like scaffolding for brain cells begin to twist and tangle. The cell is damaged and eventually dies. But the tangled proteins remain in the brain even after the dead neuron has been cleared away.(10,14) And inflammation might be the culprit causing the long protein fibers to start tangling.(15)

The consequence of these abnormalities of protein in the brain is more than the cell death they cause. They also act as roadblocks, interfering with electrochemcial messengers being shot from cell to cell. Therefore, the remaining healthy cells’ activity is diminished as well.

Research of identical twins has repeatedly shown that if one twin has Alzheimer's disease, the other has a 60% chance of developing the disease, too. Scientists from the Karolinska Institute in Stockholm, Sweden, looked at information from 20,000 twins collected in the 1960s and found 109 pairs of siblings where only one twin had been diagnosed with Alzheimer's. When the Swedish researchers analyzed data about the twins' health, they found the twin with Alzheimer's disease almost always had chronic gum disease. While bleeding gums are definitely not the cause of Alzheimer's disease, the inflammation that plays a large part of chronic gum disease may signal an inflammatory process stuck in overdrive.(16)

In fact, the inflammatory process might occur years before the onset of Alzheimer's, and be the result of any number of infections people can contract. That's why current research is searching for ways to protect brain cells from inflammation. And why some countries have low rates of Alzheimer's disease, like India.

  • Why curry? Couldn't other lifestyle differences account for the low rates of Alzheimer's disease in India?

That's a good question. When researchers begin studying a disease, like Alzheimer's, they look for trends to help them determine how and why the disease occurs. For example, we all now know the connection between cigarette smoking and lung cancer. But, it wasn't until the 1930's that doctors noticed the trend for cigarette smokers to have more lung cancer than people who didn't smoke.(17)

So it has been with researchers studying Alzheimer's disease. They know Alzheimer's disease has an important connection to inflammation. They also know turmeric reduces inflammation. And when researchers noticed these trends - that people in India eat high amounts of curry from turmeric and have very little Alzheimer's disease - they began to theorize that turmeric might be able to prevent or even treat the illness. And the research they designed around these trends has unequivocally found turmeric to be one common denominator.(18-21)

  • What have the turmeric studies shown so far?

Simply amazing findings are coming from curry research. Not only does turmeric slow down cancer growth, it's also been found to correct the cystic fibrosis defect in mice, help prevent the onset of alcoholic liver disease, and may slow down other serious brain diseases like multiple sclerosis.(22)

Researchers from the University of California Los Angeles (UCLA) studying turmeric have found it to be more effective than the drugs currently being investigated for Alzheimer's disease treatment and prevention. The researchers have discovered the actual structure and shape of turmeric allows it to penetrate the blood-brain barrier effectively and bind to beta amyloid.(23) Other research findings shows turmeric helps remove beta-amyloid that's already built up in the neurons.(24) Turmeric helps maintain healthy brain cellular metabolism, helps the cells repair themselves, and keeps the cells connected to each other.(25,26) In other words, turmeric helps brain cells stay healthy.

And now the UCLA Alzheimer's Disease Research Center (ADRC) is using turmeric in clinical trials and studying the effect of this powerful spice in patients diagnosed with this devastating disease. Clinical trials are the gold standard of medical research. But it's rare in Alzheimer's disease. And it's even more rare when all-natural herbs and spices like turmeric are used in hopes that positive benefits will be discovered. The head of UCLA's research team was recently interviewed and stated that setting out to hopefully prove turmeric's ability to prevent and treat Alzheimer's disease was “tremendously exciting.”(27)

  • I recently read that one of the nonsteroidal anti-inflammatory drugs (NSAID) was found to prevent Alzheimer's disease. Is this true?
Scientists recently studied ibuprofen, one of the NSAIDs investigated for Alzheimer's Disease Prevention.(28) Ibuprofen belongs to a family of drugs that includes naproxen, indomethacin, nabumetone, and several others. These drugs are used most often to get rid of headaches, mild arthritis, and other kinds of pain and inflammation.(29) In the studies, the average dose of ibuprofen was 800mg a day. Patients took the product for two years. While the results suggested that ibuprofen might reduce the risk of developing Alzheimer's, ibuprofen's side effects are too harmful to be a valid lifelong prevention aid treatment.(28) Ibuprofen, like other NSAIDs, can cause gastrointestinal bleeding when used at high dosages over a long period of time. Long term use of ibuprofen can also lead to analgesic nephropathy, a kind of kidney damage caused by NSAIDs.(29)

As we discussed earlier, turmeric appears to block and break up brain plaques that cause the disease and helps reverse some of the damage already present.(19,21,26) Ibuprofen does not provide any protection against free radical damage. No anti-inflammatory medicine can do this.(29)

  • If I eat curry will I be protected against Alzheimer's disease? There aren't many foods or recipes I make that require curry, do I need to eat it every day? And how much do I need?

If you enjoy Indian cuisine, by all means, enjoy these delicious foods. You'll benefit your brain and your appetite. But you make a good point, American meals rarely contain curry. That's why supplements that contain extracts are suddenly quite popular. In fact, there are numerous turmeric/curcumin supplements on the market today.

But like all nutritional supplements, some turmeric supplements are superior to others. You need to read their labels to make sure the turmeric extract you are buying will provide the protection you need. Look for high-potency turmeric extract from turmeric (Curcuma longa) rhizome. And make sure the extract is standardized to contain 90% curcuminoids, the active ingredient in turmeric responsible for the positive research findings.


Researchers once thought that preventing for Alzheimer's disease would elude them for decades. In fact, several scientists privately speculated the disease might never be ameliorated. They thought the origin of the disease was too complex and the symptoms of the disease were too profound. That's why the ongoing research on turmeric is so exciting. A safe, natural, and effective way to protect against Alzheimer's disease almost seems too good to be true. But, the nation of India and its low incidence of Alzheimer's disease are proof these are not just fluke findings - making turmeric extract a supplement to remember.


1. Jha S, Patel R. Some observations on the spectrum of dementia. Neurol India. 2004;52:213-4.

2. Vas CJ, Pinto C, Panikker D, et al. Prevalence of dementia in an urban Indian population. Int Psychogeriatr. 2001;13:439-50.

3. The Alzheimer's Disease Fact Sheet. Alzheimer's Disease Education & Referral Center. A service of the National Institute of Aging. Accessed on September 8, 2005. Available at: ml#Contents.

4. Chandra V, Pandav R, Dodge HH, et al. Incidence of Alzheimer's disease in a rural community in India: the Indo-US study. Neurology. 2001;57:985-9. 5. Ringman JM, Frautschy SA, Cole GM, Masterman DL, Cummings JL. A potential role of the curry spice curcumin in Alzheimer's disease. Curr Alzheimer Res. 2005;2:131-6.

6. Curcuma longa (turmeric). Monograph. Altern Med Rev. 2001;6 Suppl:S62-6.

7. Sharma RA, Gescher AJ, Steward WP.Curcumin: The story so far. Eur J Cancer. 2005;41:1955-68.

8. Weber WM, Hunsaker LA, Abcouwer SF, Deck LM, Vander Jagt DL. Anti-oxidant activities of curcumin and related enones.Bioorg Med Chem. 2005;13:3811-20.

9. Karunagaran D, Rashmi R, Kumar TR. Induction of apoptosis by curcumin and its implications for cancer therapy. Curr Cancer Drug Targets. 2005;5:117-

10. Curtis SM, Porth CM. Alzheimer's disease. In: Porth CM. Pathophysiology: Concepts of Altered Health States. 5th ed. Philadelphia, Pa: Lippincott; 2002: 914- 917.

11. Fryer JD, Holtzman DM. The bad seed in Alzheimer's disease. Neuron. 2005;47:167-8.

12. Kranenburg O, Bouma B, Gent YY, et al. Beta-amyloid (Abeta) causes detachment of N1E-115 neuroblastoma cells by acting as a scaffold for cell-associated plasminogen activation. Mol Cell Neurosci. 2005;28:496-508.

13. Morgan C, Colombres M, Nunez MT, Inestrosa NC. Structure and function of amyloid in Alzheimer's disease. Prog Neurobiol. 2004;74:323-49.

14. Liazoghli D, Perreault S, Micheva KD, Desjardins M, Leclerc N. Fragmentation of the Golgi apparatus induced by the overexpression of wild-type and mutant human tau forms in neurons. Am J Pathol. 2005;166:1499-514.

15. Minghetti L. Role of inflammation in neurodegenerative diseases. Curr Opin Neurol. 2005;18:315-21.

16. Andel R, Crowe M, Pedersen NL, Mortimer J, Crimmins E, Johansson B, Gatz M. Complexity of work and risk of Alzheimer's disease: a population-based study of Swedish twins. J Gerontol B Psychol Sci Soc Sci. 2005;60:P251-8.

17. Heady JA, Kennaway EL. The increase in deaths attributed to cancer of the lung. Br J Cancer. 1949;3:311-20.

18. Park SY, Kim DS. Discovery of natural products from Curcuma longa that protect cells from beta-amyloid insult: a drug discovery effort against Alzheimer's disease. J Nat Prod. 2002;65:1227-31.

19. Yang F, Lim GP, Begum AN, et al. Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. J Biol Chem. 2005;280:5892-901.

20. Ono K, Hirohata M, Yamada M. Ferulic acid destabilizes preformed beta-amyloid fibrils in vitro. Biochem Biophys Res Commun. 2005;336:444-449.

21. Ono K, Hasegawa K, Naiki H, Yamada M. Curcumin has potent anti-amyloidogenic effects for Alzheimer's beta-amyloid fibrils in vitro. J Neurosci Res. 2004;75:742-50.

22. Aggarwal BB, Shishodia S. Suppression of the nuclear factor-kappaB activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y Acad Sci. 2004;1030:434-41.

23. Yang F, Lim GP, Begum AN, et al. Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. J Biol Chem. 2005;280:5892-901.

24. Giri RK, Rajagopal V, Kalra VK. Curcumin, the active constituent of turmeric, inhibits amyloid peptide-induced cytochemokine gene expression and CCR5-mediated chemotaxis of THP-1 monocytes by modulating early growth response-1 transcription factor. J Neurochem. 2004;91:1199-210.

25. Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J Neurosci. 2001;21:8370-7.

26. Cole GM, Morihara T, Lim GP, Yang F, Begum A, Frautschy SA. NSAID and Antioxidant Prevention of Alzheimer's Disease: Lessons from In Vitro and Animal Models. Ann N Y Acad Sci. 2004;1035:68-84.

27. The Univerity of California at Los Angeles (UCLA) Alzheimer's Disease Research Center (ADRC) Current studies: Mild to Moderate Alzheimer's Disease and Curcumin. Information available at the ADRC Website: asp.

28. Pasinetti GM. From epidemiology to therapeutic trials with anti-inflammatory drugs in Alzheimer's disease: the role of NSAIDs and cyclooxygenase in betaamyloidosis and clinical dementia. J Alzheimers Dis. 2002;4:435-45.

29. What You Need to Know About Nonsteroidal Anti-Inflammatory Medications (NSAIDs). The Cleveland Clinic Health Information Center. Accessed on September 8, 2005. Available at: ealthinfo/ docs/0700/0714.asp?index=4901.

Tags:  alzheimer's  tumeric 

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Is Your Medication Robbing You of Nutrients?

Posted By Administration, Friday, August 20, 2010
Updated: Friday, April 18, 2014

by Hyla Cass, MD 3308079338_c8c107bc7f_b   


A little known but potentially life-saving fact is that common medications deplete vital nutrients essential to your health. Here's a practical guide to avoid drug-induced nutrient depletion, and even replace your medications with natural supplements.


We have been called a pill-popping society, and statistics bear this out. Nearly 50 percent of American adults take at least one prescription drug, and 20 percent take three or more. In a survey(1), more than half of those over 65 and 30 percent of people 45 to 65 used at least three prescription drugs in a one-month period. With our increasing reliance on medications comes nutrient depletion, a problem we can't ignore. Every medication, including over-the-counter drugs, will drain the body of specific nutrients. On top of this, most Americans are already suffering from nutrient depletion. In fact, many of the conditions we see in everyday practice may actually be related to this deficiency.

The good news is that with the right supplements, you can avoid depletion side effects, and even better, you may be able to control and prevent chronic diseases, such as diabetes, cardiovascular disease and osteoporosis.


A Common Scenario

I have seen case after case of patients who have experienced nutrient loss from taking prescribed medications. Too often, neither the patients nor their doctors were aware that the cause of symptoms was the medications themselves.

For example, a 57-year-old retired schoolteacher, Kathy, was being treated by her internist with three medications: the thiazide diuretic, Diuril, for high blood pressure; Fosamax for osteoporosis; and the beta-blocker, Tenormin, for heart palpitations.

She was referred to me, an integrative psychiatrist, because she suffered from fatigue, anxiety, depression and insomnia. I couldn't find an obvious psychological explanation for these symptoms, except perhaps for the stress of her physical illnesses.

The likeliest cause of her symptoms was the drugs themselves. So, rather than adding an antidepressant, an anti-anxiety pill or sleeping agent, I checked the known nutrient depletions associated with these medications. Lab results confirmed that Kathy was deficient in three essential minerals: magnesium, potassium and zinc.

Any one of her three medications could deplete potassium and magnesium, causing arrhythmias, hypertension, fatigue and depression. The diuretic also could be depleting zinc. Her internist agreed that he would continue to oversee her medications while I supervised her nutritional regimen.

Daily doses of magnesium, zinc and potassium, in addition to a high-potency multivitamin, resolved Kathy's "psychiatric" symptoms. Once her mineral levels were restored, her energy and mood were back to normal. She was not only spared the burden of an additional medication, but was able to lower the doses of the three she was taking.

I see cases similar to Kathy's more frequently than I'd like. Physicians will often tell these patients that their symptoms are "part of the illness" or "just signs that they're getting older." They then prescribe an additional drug or two for the side effects, further compounding the problem.

To understand the role of medications in nutrient depletion, we must first understand the variety of nutrient-depleting mechanisms in pharmacy.

Many drugs, such as the stimulants Ritalin (methylphenidate) and Adderall, are prescribed for attention deficit disorder. These can reduce appetite. This, in turn, decreases the intake of beneficial nutrients. Some antidepressants also tend to have this appetite-reducing effect.

On the flip side, a drug can reduce nutritional status by increasing the desire for unhealthy foods, such as refined carbohydrates. Many of the neuroleptics (antipsychotic drugs) and some antidepressants cause insulin resistance or metabolic syndrome, with resulting blood sugar swings. Patients then crave simple carbohydrates, such as sugar, bread and pasta. Steroid drugs, including those given by an inhaler, can create similar issues as well.

Certain medications reduce the absorption of nutrients. In passing through the gastrointestinal tract, drugs often bind to specific nutrients before they're absorbed into the bloodstream. The antibiotic, tetracycline, for example, can block absorption by binding with minerals such as calcium, magnesium, iron and zinc in the GI tract.

Weight loss drugs and cholesterol lowering medicines similarly bind to fats, preventing them from being absorbed. Drugs that treat acid reflux or heartburn raise the pH environment of the upper GI tract, which reduces absorption of needed vitamins and minerals. This is especially problematic among the elderly, who often are already low in stomach acid.

Nutrients are essential to the metabolic activities of every cell in the body. They're used up in the process and need to be replaced by new nutrients in food or supplements. Some drugs deplete nutrients by speeding up this metabolic rate. These drugs include antibiotics (including penicillin and gentamicin) and steroids, such as prednisone and the gout medication, colchicine.

Other drugs block the nutrients' effects or production at the cellular level. In addition to the intended effect on enzymes or receptors, medications can influence enzymes or receptors that help process essential nutrients. For example, widely prescribed statin drugs block the activity of HMG-CoA, an enzyme that's required to manufacture cholesterol in the body. This action also depletes the body of coenzyme Q10, which requires HMG-CoA for its production. This has a serious negative impact on muscle and heart health.

Drugs also can increase the loss of nutrients through the urinary system. Any drug that does this can drain the body's levels of water-soluble nutrients, including B vitamins and minerals, such as magnesium and potassium. The major offenders are medications to treat hypertension, particularly the diuretics that reduce blood pressure by increasing the volume of water flushed out of the body.

Drug-induced nutrient depletion is far more common than we think. In evaluating patients' symptoms, doctors must assess whether symptoms are due to the illness, to side effects of the drugs or to drug-induced nutrient depletion. Considering the inadequate nutrition of most people, we must remember that the illness itself may be due, in part, to nutrient deficiency. To cover all bases, it is easiest to provide baseline coverage: a daily high potency multivitamin mineral formula, CoQ10 (200 mg), omega-3 fatty acids (2 grams) and additional vitamin D and probiotics, especially if you've taken antibiotics.

The bottom line: As physicians, we must look more deeply and determine underlying causes to determine whether drugs are harming patients, and what we can do to reverse these effects. As a consumer, be aware of these drug-nutrient depletions, and do what you can to avoid taking medications whenever you can, using natural products instead.

1. Centers for Disease Control and Statistics. Health United States 2006. Accessed via

Tags:  side effects 

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Was Your Child Mislabed with ADHD?

Posted By Administration, Wednesday, August 18, 2010
Updated: Friday, April 18, 2014

by Gina Nick, NMD, PhD

4355506063_4105c0c877_oA new study released by Michigan State University found that nearly 1 million children have been misdiagnosed with attention deficit hyperactivity disorder (ADHD).  The reason, the study found, was that kids who are youngest in their grades have a 60% greater chance of being diagnosed with ADHD. Nothing to do with brain chemistry, or the genuine need for medications.  Simply due to their age. The details of this study were just published in USA Today.


There are beneficial naturopathic treatments for those labeled with ADHD. The beauty of Naturopathic Medicine is that doctors are treating the individual. Even if your child was diagnosed with ADHD,  a licensed Naturopathic Medical Doctor will work on the underlying cause of the behavioral challenges and not simply treat the label your child was given by writing a script for Ritalin or other popular ADHD medication.  This individualized treatment helps to prevent misdiagnosis and unnecessary treatments with unknown long-term effects to a child’s developing brain and nervous system. Let’s focus on what is in the best interest of the children, now and in the future.  Finding a doctor who takes the time to get to know your child, run appropriate lab tests to pinpoint the imbalances, and is focused on addressing the underlying cause of your child’s behavioral challenges is a reasonable place to start.


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Hair Supply - Here Today, Gone Tomorrow

Posted By Administration, Friday, August 13, 2010
Updated: Friday, April 18, 2014

by Joel Lopez, MD, CNS 4336272863_3653acf839_b  

Why is it that we’re seeing younger people getting hair loss at such an early age? Is it just a genetic issue or does it have to do with environmental factors as well? I believe that it’s due to both. Genetic causes of chronic degenerative disease is only about 3-4%, compared to greater than 90% due to environmental causes.

There’s a lot we can do to prevent or even reverse hair loss. We have to know the factors that lead to this condition. One, there’s the issue of poor circulation. Our hair needs to be nourished. Poor circulation means less nutrients going to the hair follicles. What causes poor circulation? Dietary factors such as intake of trans-fats or hydrogenated oils as well as calcium build-up along the arterial lining can do that. Poor nutrition also leads to hair loss. Where do you think our hair comes from? It comes from our food. Hair is primarily protein. Therefore, an adequate intake of amino acids should lead to a full head of hair. But, it’s not just that. An adequate amount of certain vitamins, minerals and glycosaminoglycans are also needed for healthy hair. Nutritious food should contain adequate nutrients. However, this is not always true because certain produce, esp. ones that are produced through commercial, chemical farming are nutritionally deficient. Produce farmed bio-dynamically and not just organically, should contain adequate amounts of nutrients to help our body renew itself (and that includes the hair).

What about personal products that damage the hair or hair follicles? There’s a substance in hair gels or products that could actually clog the hair follicles and cause them to ultimately die. The one implicated the most is a chemical called PVP coplymer, a petrochemical product. Avoid this at all costs. There are other chemicals that could cause damage to cells in general such as pthalates and sodium lauryl/laureth sulfate. Just notice how more companies are touting that they don’t contain these products.

Another cause of hair loss is hormonal imbalance. Undiagnosed thyroid issues could cause hair loss. A testosterone metabolite called DHT could cause hair loss, thus the popularity of synthetic DHT blockers such as Propecia or Avodart. A more natural way to influence testosterone metabolism is through the use of zinc supplements (which by the way is a very common nutritional deficiency). Other natural DHT blockers include saw palmetto, lycopene (from tomatoes), pygeum and stinging nettle. Low testosterone levels in men as well as low estrogen levels in women could also lead to hair loss. Isolated HGH deficiency could cause regeneration and repair to slow down as we age. That means, less production of new tissue, including our hair.

What do you do to improve HGH levels? Besides exercise, there are amino acids that stimulate HGH release from the pituitary. The most effective one for people over the age of 40 is L-glutamine. Goji berries has been used in Traditional Chinese Medicine to stimulate HGH release from the pituitary. Otherwise, a peptide called HGHRH (analogue) could also be used. I found this as effective as HGH, with less side effects.

What are other natural remedies that could stimulate hair growth? An Ayurvedic treatment includes the use of neem hair oil. Traditional Chinese medicine may recommend fo-ti pr he she wou. Essential oils that stimulate hair growth include therapeutic-grade peppermint, cedarwood, rosemary, lavender, thyme and sandalwood. Minoxidil works for some people but it does work better combined with substances such as retin-A, aldactone, progesterone, azelaic acid, copper peptides, SOD, and copper-zinc binding peptides.

Procedures one should consider before the last resort (hair transplant) include the use of low level laser therapy and the use of a micro-dermaroller. Consult with your holistic health care practitioner before incorporating any of the above suggestions.

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Resveratrol for Polycystic Ovarian Syndrome

Posted By Administration, Thursday, August 12, 2010
Updated: Friday, April 18, 2014

by Fiona McCulloch, ND 

3944981634_216f370e16Polycystic ovarian syndrome is a complex condition involving multiple hormonal components.  Treatment of this disease therefore must be multifold:   low glycemic index diets, exercise, therapies to reduce excessive tissue androgens and estrogens, enhancement of insulin resistance and antioxidant status, and improvement of luteal phase health and progesterone balance. In this article I will discuss one newly studied therapy for PCOS : resveratrol.  It can greatly effect the health of the ovary in PCOS and can be an excellent addition to an overall protocol for the treatment of this condition.

Different women will present with different symptoms, degrees, and signs of PCOS, and each woman will require very customized treatment.  In women with PCOS  and especially in those who have enlarged ovaries or multiple cysts in the ovaries, the theca-interstitial cells of the ovary are especially prone to growing excessively.   These cells do not undergo the normal cycle which allows the cells to die off and get replaced by new cells (known as apoptosis) .

The theca interstitial cells of the ovary are responsible for producing male hormones which are normally required for healthy ovarian function.  However in PCOS , the large amount of these cells causes a large amount of male hormones to be produced,  causing problems with normal ovulation.  This often results in delays in ovulation (and therefore in menstruation)  or lack of ovulatory cycling altogether in more severe cases.   These hormonal changes also greatly reduce egg quality and health.

There are two causes for the excessive overgrowth of these theca interstitial cells of the ovary  1) high levels of oxidative stress and 2) high levels of insulin in the local tissues. Both of these factors play a great role in the pathology of polycystic ovarian syndrome.

A new study just released in April 2010 indicates that resveratrol (a antioxidant compound found in grapes) has powerful benefits in this type of condition.  Although other forms of grape antioxidants have long been used to treat infertility, it is the oligomeric proanthocyanadin (also known as OPC) component that has been traditionally used.  The effect of resveratrol however is different from the effects of OPCs, which are both antioxidants and pro circulatory compounds.   Resveratrol does reduce oxidative stress like many other types of antioxidants,  but importantly, it is also an antiproliferative compound which is well known to reduce growth of and  induce cell death in cancer cells (another form of cell which proliferates excessively and out of bounds of healthy control).

This study, completed by the University of California School of Medicine, Department of Gynecology and Obstetrics, investigated the effect of resveratrol on the theca interstitial ovarian cells of rats.    The cells were cultured with and without resveratrol and/or insulin.  This was done in order to gauge the effect of resveratrol on these abnormally growing cells without other factors, and also in the presence of insulin, a factor which is high in patients with PCOS and which is known to further stimulate unhealthy cellular growth.

The results showed that the ovarian cells cultured in resveratrol alone showed a potent, concentration dependent decrease in the abnormal growth of cells.  In the ovarian cells cultured with both resveratrol and insulin (mimicking the common conditions of PCOS) it was found that the resveratrol was able to counter the negative effects of the insulin on the ovarian cells and allow them to undergo the normal cell death process required for healthy ovarian function.

This versatile and powerful compound found in grapes may be a promising new treatment for PCOS (this disease coincidentally, often causes a ” bunch of grapes ” appearance of the ovaries when examined by ultrasound, due to the large number of cysts or accumulated follicles).  Resveratrol may prove to be a very effective part of multi faceted protocols to enhance ovarian health and restore normal ovarian hormone production for the millions of women worldwide with PCOS.


Effects of resveratrol on proliferation and apoptosis in rat ovarian theca-interstitial cells.
Wong DH, Villanueva JA, Cress AB, Duleba AJ.
Mol Hum Reprod. 2010 Apr;16(4):251-9.


Effects of insulin and insulin-like growth factors on proliferation of rat ovarian theca-interstitial cells.
Duleba AJ, Spaczynski RZ, Olive DL, Behrman HR.
Biol Reprod. 1997 Apr;56(4):891-7.

Cytotoxic Effect of Wine Polyphenolic Extracts and Resveratrol Against Human Carcinoma Cells and Normal Peripheral Blood Mononuclear Cells.
Matić I, Zižak Z, Simonović M, Simonović B, Gođevac D, Savikin K, Juranić Z.
J Med Food. 2010 May 18.

Proliferation of ovarian theca-interstitial cells is modulated by antioxidants and oxidative stress.
Duleba AJ, Foyouzi N, Karaca M, Pehlivan T, Kwintkiewicz J, Behrman HR. Hum Reprod. 2004 Jul;19(7):1519-24.

Tags:  polycystic ovarian syndrome  resveratrol 

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Staying Ahead of the Curve on Parkinson's Disease

Posted By Administration, Monday, August 9, 2010
Updated: Friday, April 18, 2014

by Zina Kroner, DO 4090198486_ef681509fb_o   

More recently, doctors are being urged to treat dementia more aggressively in Parkinson's patients, as it would optimize quality of life for the patients and their caregivers. It is established that one third of patients with Parkinson’s disease experience dementia. Cognitive impairments are the hallmark features, including decreased attention span, executive functioning and memory deficits. Obtaining a legitimate diagnosis of dementia can be quite tricky in that symptoms may widely fluctuate and therefore the diagnostic instruments that physicians use to diagnose Parkinson’s dementia may not always give reliable results.  Research is conflicting at this point as to which is the best medical agent to use in this population. 


Optimize Diet 

There are multiple safe nutritionally oriented treatments that patients may engage in to help prevent early onset dementia as it is related to Parkinson’s disease.  First and foremost, optimization of diet is critical. There is much research to suggest that a diet that is high on the glycemic index scale can exacerbate dementia.  Insulin resistance, associated with a diet that is chronically high on the glycemic index, has been associated with Alzheimer’s disease. The connection has been labeled type 3 diabetes by some. (See my published article under the References section of my website on this topic).

Low Glycemic Index, No Pesticides, No MSG 3013741860_ab25d8ce03_z  

Eating organic, MSG and pesticide free foods that can exacerbate both Parkinson’s as well as dementia is important.  Remember that MSG can trigger glutamate receptors in Parkinson’s and non-Parkinson’s patients alike.  Following a Mediterranean style diet that is high in unheated extra virgin olive oil, fish and poultry, nuts, vegetables, low glycemic index fruits, whole grains that are gluten free and unprocessed foods is key.   

Just Do It


3218300813_2a10d6453c_bAdding a daily exercise component is imperative. Exercise can trigger dopamine levels to rise, help with coordination, drive down cortisol, improve insulin resistance, and help with mental acuity. These are all essential when hoping to help prevent dementia and improve Parkinson’s symptoms. Exercise should include weight bearing exercise as well as core bodywork.



The adrenal hormone DHEA has been shown to boost dopamine levels. There is also a significant amount of research pointing to DHEA helping with improvement in memory in dementia patients. DHEA is ever present in brain tissue and helps to offset the negative effects of cortisol.  It is, however, a precursor to many of the other hormones and needs to be used judiciously and under medical supervision. 

Follow an Anti-Inflammatory Program

Low grade chronic inflammation may be a precursor to neurodegenerative disease. An excellent anti-inflammatory program, including diet and supplements may help to quiet the inflammation down. 

Polyphenols, excellent antioxidants found in green tea, have recently been studied to see if they modify the course of Parkinson’s.  The Chinese study enrolled 410 untreated people with Parkinson’s disease and were randomized to receive 0.4g, 0.8g, or 1.2 g of green tea polyphenols daily. As a reference, 2 cups of green tea contain approximately 300mg of polyphenols.  At 6 months a significant improvement was noted in each dosage category based on the Unified Parkinson's Disease Rating Scale. At 12 months, however, unexplainably, the scores did not differ from placebo. Improvements were more profound for those with a greater severity of disease.  There were no notable side effects except for insomnia for those not accustomed to green tea intake. 

The reduction of oxidative stress on neurologic tissue in Parkinson’s as well as dementia patients is important.  Utilization of polyphenols, vitamin C, tocotrienols, bioflavanoids, proanthocyandins from grape seed extract, coenzymeQ10, and curcumin may have a beneficial effect.   

Tags:  parkinson's disease 

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Statins' Laundry List

Posted By Administration, Sunday, August 8, 2010
Updated: Friday, April 18, 2014

by Zina Kroner, DO

4700292186_7114d6584f_o (1)According to a recent study not funded by a pharmaceutical company, in the journal Lancet, use of statins (Lipitor, zocor, etc) is associated with a small risk of developing diabetes.  When looking at 90,000 subjects in this meta-analysis, it was found that there was a 9% increase in diabetes risk as compared to controls. This association was of greater significance with increasing age. 

How does this affect you, statistically speaking?  

Well, for every 255 patients treated with a statin medication for four years, there is the potential, according to the authors of this study, to produce one additional case of diabetes.

Add it to the Laundry List

This is yet another adverse effect added to statins’ already long list of side-effects.  It means that physicians as well as patients have to be cognizant of this fact and monitor for signs and symptoms of glucose imbalance on a regular basis.  

Remember that statin drugs are effective at reducing overall cardiovascular risk, so cardiologists will argue that the benefits of statins far outweigh the risks.  From a conventional standpoint, it is, therefore, not recommended to change the existing indications for statin therapy in the setting of cardiovascular risk prevention.  

Tags:  statin 

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Overcoming Pre-Menstrual Syndrome Naturally

Posted By Administration, Tuesday, July 27, 2010
Updated: Friday, April 18, 2014

3631665064_c3604847b5_oby Hyla Cass, MD


Our mothers once called them "women's problems." Now we know that these mood swings and physical changes, from PMS to menopause, are all part of a delicate balance among our various hormones. In my years of practicing integrative medicine, I have helped hundreds of women overcome PMS and menopausal symptoms naturally, and here's how.

Let's start by defining hormones. They are chemical messengers secreted by any one of the body's endocrine (ductless) glands. They travel through the bloodstream, telling various systems what to do. Besides reproductive functions, hormones affect virtually every body system from digestion to metabolism to hair growth.

All women have the same hormones but in varying quantities, making your own hormonal profile as unique as your fingerprint. When your hormones are in harmony, you will have predictable menstrual cycles --and moods. When out of balance, you will have irregular cycles and a host of symptoms, from bloating, cramps, weight gain and acne to food cravings, irritability and depression. Perimenopause, the transition to menopause, which can start as early as your late 30's, often causes an increase in PMS. In fact, many women report experiencing PMS for the first time at that point. Also common in peri-menopausal women, is a loss of libido, due to a dip in testosterone which governs sexual desire, and of course, those hot flashes and night sweats, which make sex the last thing on your mind!

Medical Management

For a full picture of your hormonal status, we need to check levels of estrogen, progesterone, DHEA-S and testosterone in blood, saliva, or urine, taken on day 19-21 of the cycle. For perimenopausal women, I also order FSH (follicule stimulating hormone) and LH (luteinizing hormone) blood tests to assess ovarian function. I will check cortisol levels (saliva test) and thyroid hormones (blood test), too, since they are a part of the overall hormone symphony.

You can find home testing kits online. Take these tests on days 19-21 of your cycle, with day one being the first day of your period. If you are post-menopausal, it won't matter when you take the tests. If you're irregular, do your best to estimate the appropriate date.

Hormone Therapy

If testing reveals that your hormone levels to be below the normal range, it may be due to perimenopause or other physiological factors. Faced with fluctuating hormones, doctors have traditionally prescribed synthetic hormone replacement therapy (HRT), such as Premarin (from pregnant mares' urine) and Prempro (Premarin plus synthetic progesterone), to correct imbalances. The recent Women's Health Initiative study showed that women taking this form of HRT had 27 percent more heart attacks, a higher rate of breast cancer, 38 percent more strokes and double the number of blood clots. There are safer ways to balance hormones successfully, ranging from supplements and herbs to bio-identical hormone therapy.

Natural Ways to Balance Sex Hormones

The first step to balancing your hormones is a clean diet:

• Eat fewer animal products, with lots of vegetables, including raw broccoli and other 
cruciferous veggies 
• Reduce or eliminate caffeine, alcohol, nicotine and sugar. 
• Reduce or eliminate high-fat dairy products. 
• Eliminate as much processed food as possible
• Reduce salt intake. 
• Eat small, regular meals.

Yoga and meditation are helpful for PMS sufferers because they work on the nervous system to help balance hormones.


Supplements for PMS:

I give my patients magnesium (100 mg two to three times daily) and vitamin B6 (25-100 mg) to relieve irritability and tight muscles as well as premenstrual water retention.

Another important nutrient is GLA, an omega-6 fatty acid which also helps reduce the water retention, breast tenderness and moodiness associated with PMS, likely by it's action on the hormone prolactin. GLA is found in borage oil (1500 mg of borage twice daily), black currant seed or evening primrose oils.

The herb, Chasteberry (Vitus Agnus Castus), helps to balance the hormone, progesterone, relieving symptoms of PMS and heavy or irregular periods as well. Dose is 50-200 mg daily depending on symptoms.
 Do not take if you're pregnant.

The herb, Dong Quai, helps to balance the hormone estrogen. Like Vitex, the dose is 50-200 mg daily depending on symptoms and also do not take if you're pregnant.

Another useful nutrient is the amino acid, 5-HTP (5-hydroxytryptophan) 500-200 mg daily, depending on your individual needs. It helps to raise levels of the feel-good and calming brain chemical, serotonin, which is often low in PMS sufferers.

These nutrients plus wild yam a source of natural hormone production, can all be found in the formulation, PMS Balance. I have had many women report almost immediate relief upon taking this or a similar formula. Others may take a month or two to feel the full effects.

With menopausal symptoms, I may also add black cohosh and red clover extract. While there was a recent study that claimed that black cohosh didn't work, it was in fact, flawed, and contradicted numerous well-done studies that found it to be very effective. I have also discovered a remarkable new product called FemmePhase. Even the majority of my hard-core hot flashers have found relief with it.

Bio-identical Hormones

When the nutrients aren't quite doing the job, you can add over-the-counter natural progesterone cream (up to 30 mg daily) for one week prior to your period. This is a maximum of 3 percent progesterone, or 30 mg per 1 gram dose.

I may also prescribe higher dose bio-identical hormones for my patients. The progesterone is often 10 percent, which is three times as strong as the over-the counter dose. Made from highly purified derivatives of soy and wild yams, these formulas are carbon copies of your own natural hormones. Prescription strength bio-identical hormones are available only from compounding pharmacies, and are prescribed by your doctor. Doses are based on your individual hormonal needs as determined by your lab tests.

As I say repeatedly - "you don't have to live with PMS/peri-menopausal symptoms." This applies to both the woman herself and her long-suffering loved ones. This information should help you take care of most cases of PMS and peri-menopausal symptoms. I have many grateful women, and their partners, for whom PMS has truly become a thing of the past.

Tags:  fertility  Infertility  menstrual 

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Best Alternatives to Statins for Treating Hyperlipidemia

Posted By Administration, Friday, July 23, 2010
Updated: Friday, April 18, 2014

Clinical Question

When statin therapy is not tolerated, what are the best alternative treatments for patients with hyperlipidemia?

Evidence-Based Answer

Most alternatives to statin therapy reduce cholesterol levels but do not consistently demonstrate a reduction in cardiac-related and all-cause mortality in patients with or without coronary heart disease (CHD). Fibrates and niacin decrease the risk of major coronary events; however, no statistically significant reductions in mortality have been shown. (Strength of Recommendation [SOR]: A, based on systematic review of randomized controlled trials [RCTs]).

Resins decrease cardiovascular mortality but not total mortality. (SOR: A, based on review of RCTs).

The effects of ezetimibe (Zetia) on cardiovascular outcomes and mortality are unknown. (SOR: C, based on a single RCT with disease-oriented evidence).

Omega-3 fatty acid supplementation does not clearly demonstrate reductions in mortality. (SOR: A, based on two meta-analyses of RCTs).

There is insufficient evidence to recommend the use of herbal therapy for the treatment of hyperlipidemia. (SOR: A, based on a systematic review of RCTs).

Evidence Summary

A literature search found one systematic review that included 97 RCTs comparing different classes of antilipidemic therapies.1 Other studies focused on specific therapies and included one high-quality systematic review of 12 RCTs, 22 prospective cohort studies, four case reports, and one cross-sectional study evaluating cardiovascular outcomes for omega-3 fatty acid supplementation; one systematic review of 27 RCTs on garlic; and one systematic review of 25 limited-quality RCTs of 11 herbal products.24 Additional studies included a systematic review of 48 RCTs and 41 cohort studies evaluating the effect of omega-3 fatty acid supplementation on mortality, cardiovascular disease, and cancer; a subsequent Cochrane review that addressed omega-3 fatty acid supplementation for the prevention and treatment of cardiovascular disease; and a meta-analysis of 53 RCTs evaluating fibrates and 30 RCTs evaluating niacin therapy.57


A meta-analysis of medications that increase high-density lipoprotein (HDL) cholesterol levels included eight RCTs evaluating the long-term clinical end points of fibrates.7 Pooled results of these studies indicate a clinically significant reduction in coronary events (number needed to treat = 33 for four years). Reductions in cardiac-related and all-cause mortality were not significant, and noncardiovascular mortality was similar in the treatment and placebo groups (relative risk [RR] = 1.10; 95% confidence interval [CI], 0.96 to 1.26). An earlier systematic review, which included the World Health Organization Cooperative Trial on primary prevention with clofibrate (not available in the United States), showed that fibrates were associated with a small but statistically significant increase in mortality (RR = 1.13; 95% CI, 1.01 to 1.27).1


Based on a meta-analysis that included a single long-term outcome study of 2,248 men treated with immediate-release niacin, cardiovascular events were reduced by 27 percent at 10-year follow-up compared with placebo; however, it should be noted that this study had a more than 70 percent drop-out rate.7

A systematic review that included two RCTs of 3,107 patients with CHD did not demonstrate a clinically significant reduction in cardiovascular mortality in those treated with niacin (RR = 0.95; 95% CI, 0.82 to 1.10).1 In this same systematic review, which included eight RCTs of resins, chole-styramine (Questran) and colestipol (Coles-tid) demonstrated significant reductions in cardiovascular death in the treatment groups (RR = 0.70; 95% CI, 0.5 to 0.99) but no significant reductions in overall mortality.1


A systematic review of 14 RCTs reported that omega-3 fatty acid supplementation resulted in a clinically significant reduction in overall mortality in patients with pre-existing CHD (RR = 0.77; 95% CI, 0.63 to 0.94).1 This review, however, excluded one RCT of 3,114 male patients with angina in the data synthesis. When this study was included, reduction in mortality was not statistically significant and had a wide confidence interval (RR = 0.84; 95% CI, 0.66 to 1.06). Based on a pooled estimate from a subsequent review that included this RCT, there was no significant reduction in cardiovascular events or mortality with omega-3 fatty acid treatment.5Another concern noted in this review and an associated Cochrane review was that relative risk of mortality seemed to increase with duration of treatment.5,6 Trials subgrouped by duration revealed a protective effect, with decreased deaths in trials lasting 24 to 47 months (RR = 0.84; 95% CI, 0.75 to 0.93) but a significant harmful effect in those lasting longer than 48 months (RR = 1.31; 95% CI, 1.07 to 1.59).5 This harmful effect was based on a single RCT.

An Agency for Healthcare Research and Quality (AHRQ) evidence report based on a comprehensive systematic review indicated that although some studies did show benefit with omega-3 fatty acid, there was an imbalance in the design of the studies, and data on women and the specific effects of different CHD outcomes are uncertain.2


One RCT found that treatment with ezeti-mibe (a cholesterol absorption inhibitor) resulted in an average low-density lipoprotein (LDL) cholesterol level reduction of about 18 percent; however, its effect on important patient health outcomes (e.g., mortality) is unknown.8


A high-quality systematic review on the effects of garlic on cardiovascular disease, which was conducted for an AHRQ evidence report, evaluted 37 studies.3 Although some modest short-term improvements in lipid measures were found, effects on cardiovascular outcomes were either not measured or not found. Thus, there is insufficient evidence to recommend use of garlic for the treatment of hyperlipidemia.3 Based on a systematic review of 25 RCTs, various herbal medications (guggul, fenugreek, red yeast rice, artichoke) may lower average total cholesterol by 10 to 33 percent; however, these studies are of poor quality overall, and an impact on mortality has not been established.4

Recommendations from Others

National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP-III) guidelines outline treatment goals in the management of hyperlipidemia with LDL cholesterol goals based on 10-year risk of CHD.9 Statins are the preferred treatment, and resins and niacin are options for add-on therapy or for treatment in patients with modest elevations of LDL cholesterol level. Fibrates have a higher risk profile and should be reserved for use in combination with statins or in patients with moderate or severe hypertriglyceridemia (triglyceride level higher than 500 mg per dL [5.65 mmol per L]). A scientific statement from the American Heart Association recommends that patients with known CHD should consume 1 g of omega-3 fatty acids containing eicosapentaenoic acid plus docosahexaenoic acid per day, preferably from oily fish.10

Clinical Commentary

Reducing morbidity and mortality is the objective of treating hyperlipidemia, and statins are the drugs that have been best proven to accomplish this. Lowering LDL cholesterol level by any other means is widely accepted as the “logical” alternative for patients who cannot tolerate statins. This approach is recommended by the NCEP ATP-III guidelines; however, the effect of this practice on mortality has not been demonstrated. Pharmaceutical companies certainly benefit from physicians' enthusiasm for “treating the numbers,” but this review should be a reminder that patients might not. It will be interesting to see if the Improved Reduction of Outcomes: Vytorin Efficacy International Trial or other trials now under way show the newest and most expensive nonstatin LDL-lowering drug to be any more beneficial than its predecessors.

When faced with a patient with hyper-lipidemia who cannot tolerate statins, it is important to take another look at the overall risk of cardiovascular disease and to inform the patient of the data (or lack thereof) regarding the expected benefits and risks of alternative treatments. The informed patient who previously decided to take statins based on the explanation of proven risk reduction may choose not to consent to take a medication with less certain benefit.





1. Studer M, Briel M, Leimenstoll B, Glass TR, Bucher HC. Effect of different antilipidemic agents and diets on mortality: a systematic review. Arch Intern Med. 2005;165:725–30. 

2. Balk E, Chung E, Lichtenstein A, Chew P, Kupelnick B, Lawrence A, et al. Effects of omega-3 fatty acids on cardiovascular risk factors and intermediate markers of cardiovascular disease. Evid Rep Technol Assess (Summ). 2004:1–6. 

3. Mulrow C, Lawrence V, Ackerman R, Gilbert Ramirez G, Morbidoni L, Aguilar C, et al. Garlic: effects on cardiovascular risks and disease, protective effects against cancer, and clinical adverse effects. Evid Rep Technol Assess (Summ). 2000:1–4. 

4. Thompson Coon JS, Ernst E. Herbs for serum cholesterol reduction: a systematic review. J Fam Pract. 2003;52:468–78. 

5. Hooper L, Thompson RL, Harrison RA, Summerbell CD, Ness AR, Moore HJ, et al. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review. BMJ. 2006;332:752–60. 

6. Hooper L, Thompson RL, Harrison RA, Summerbell CD, Moore H, Worthington HV, et al. Omega 3 fatty acids for prevention and treatment of cardiovascular disease. Cochrane Database Syst Rev. 2004;(4):CD003177. 

7. Birjmohun RS, Hutten BA, Kastelein JJ, Stroes ES. Efficacy and safety of high-density lipoprotein cholesterol-increasing compounds: a meta-analysis of randomized controlled trials. J Am Coll Cardiol. 2005;45:185–97. 

8. Brown WV. Cholesterol absorption inhibitors: defining new options in lipid management. Clin Cardiol. 2003;26:259–64. 

9. Expert Panal on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285:2486–97. 

10. Kris-Etheron PM, Harris WS, Appel LJ, for the American Heart Association Nutrition Committee. Fish Consumption, fish oil, omega-3 fatty acids and cardiovascular disease [published correction appears in Circulation 2003;107:512]. Circulation. 2002;106:2747–57.

Source: Bouknight, Patricia, Mackler, Leslie, Heffington, Mark. Am Fam Physician. 2007 Oct 1;76(7):1027-1029.

Tags:  hyperlipidemia  statin 

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Medication Side Effects and How to Prevent Them

Posted By Administration, Thursday, July 22, 2010
Updated: Friday, April 18, 2014

227906487_17d94931a3_oby Joel Lopez, MD, CNS

Medications are essential for certain acute conditions. There are people who take medications for chronic symptoms, however. It’s all fine and well until side effects happen. That’s why, a person’s biochemical individuality should always be taken into account when a person has to take medications long-term. A regular review of your medications should be in order, taking into account that there’s less metabolism or excretion of medications as we age.

Fortunately, there are genomic tests available that could tell you instantly and reliably on the kind of pharmacological substances which are most suitable for you. It furthermore advises you which dose grants you optimized therapeutic success.

One such lab is called Genosense in Vienna, Austria. They have a genomic test called Pharmacosensor. This test examines carefully selected polymorphisms which lead to structural changes in proteins that strongly influence the speed of metabolism in a series of pharmacological substances and also account for the accelerated or reduced transformation of harmless precursors of given medication into highly efficient substances.

If a person is unable to do this test, then at least they should be aware of possible nutritional deficiencies their medications could cause and make sure to replenish them.

One such class of medications are the antacid or ulcer medications. Nutrient deficiencies in Vitamins B12, folic acid, Calcium, Iron and Zinc could occur with the following potential health problems: anemia,depression, birth defects, increased cardiovascular risk, cervical dysplasia, heart disease, cancer risk, osteoporosis, muscle weakness, hearing loss, tooth decay, hair loss, brittle nails, loss of sense of taste or smell, and sexual dysfunction.

Another class of meds are the cholesterol-lowering agents called “statins”. They deplete the body of Coenzyme Q10. When this happens, various cardiovascular problems, a weakened immune system and low energy could occur.

Anticonvulsants could deplete the body of Vitamins D, B1, B2, B3, B6, B12, C, Magnesium, Selenium and Zinc. Potential health issues could include osteoporosis, muscle weakness, hearing loss, tooth decay, heart and blood pressure irregularities, cervical dysplasia, anemia, hair loss, depression, dermatitis, fatigue, reduced antioxidant protection, poor wound healing and skeletal problems.

My purpose is not to alarm people who take these medications but to make them aware that an integrative approach to any medical condition yields better results. It’s a good thing that we can now check for nutritional deficiencies. One such functional test is done through Spectracell. It checks for 33 nutrient deficiencies. I love this test because it takes the guesswork out of supplementation. Better yet, most PPO’s and Medicare cover for this test.

Tags:  side effects 

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Sunburn Savvy

Posted By Administration, Friday, July 16, 2010
Updated: Friday, April 18, 2014

by Andrea Purcell, ND 3792695572_9f7455f59e_b  

Summer is finally here and so are those warm healing rays. Even on the hazy days I had multiple reports of sunburn because the direct effects of the sun are less obvious. It can be deceiving but even though we can’t see the sun the Ultraviolet light still gets through. It’s important to practice safe sun to get the Vitamin D we need without the effects of sun overdose. However if you will be out too long here are some helpful tips in choosing a safe sunscreen:

Choose ingredients such as Zinc oxide or Titanium oxide. For an entire breakdown of safe sunscreens please visit, 2010 sunscreen guide.

As with everything in life moderation is essential. In case you were fooled into thinking that you could garden all day in a tank top here are a few natural health tips to make soothing the burn a little easier.

My favorite natural tools in treating sunburn involve 3 topical remedies and 3 homeopathic remedies.

In choosing a topical remedy you can select from one of the following, as it would do no good to use all three together.

1) Calendula Cream – made from an infusion of calendula flowers, it is well known for healing scrapes, repairing burned skin, and promoting healing.

2) Aloe Vera – the fresh gel from the plant or in a bottle from the health food store. Cooling & soothing to burned skin.

3) Liquid Minerals from Trace Minerals research – Apply the liquid minerals to your palm rub your palms together and rub repeatedly and deeply into the burned area. The trace minerals have a way of balancing and re-hydrating the areas of damaged skin. This can initially generate more heat and feel sharp and tingly on the skin.

The top three homeopathic remedies for burned skin are:

1) Calendula 30c – Soothing the burn and helping heal the damaged skin.

2) Cantharis 30c –Itching, burned skin, with small vesicles, scalding pain, & restlessness.

3) Apis 30c - Swollen skin, worse with hot applications, better with cold.

Dosing: 2 pellets dissolved on tongue every 2 hours over 36 hrs or until burn subsides or patient falls asleep.

My personal story: The first time I traveled to Ecuador, I was deceived by the notion that I could sit under an umbrella all day with SPF 15 and practice safe sun. Well by the time I had returned to my lodging that night I was as red as a lobster! Initially I couldn’t understand what had happened since I was technically in the shade all day but then it hit me, the Ultraviolet rays had passed right through the umbrella and had been cooking me slowly for hours. After all I was on the Equator. I promptly got out my first aid bag of natural remedies and selected Cantharis, and Apis. I promptly twisted two pellets of each out of the caps and dissolved them on my tongue, which I did every two hours until night fall. I slathered trace minerals all over the burned areas and rubbed them in deeply. Then I dressed in loose clothing and went to dinner. The next day I was still burned, less red and my skin was tight but no blisters. I continued my dosing of the remedies and the minerals for an additional 24 hours. By the third day the burn had turned into a deep tan, and I was without discomfort. Two weeks after I returned home the top layer of my skin peeled and that was it! I attribute the remedies in my kit to saving me from 2nd degree burns & blistered skin.

Tags:  skin  sun 

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Natural Solutions to Sleep Deprivation

Posted By Administration, Thursday, July 15, 2010
Updated: Friday, April 18, 2014

by Hyla Cass, MD   4521897133_8536c3ea22_b  

I'm seeing increasing numbers of patients with sleep problems, ranging from difficulty in falling asleep, to being unable to sleep soundly through the night. Rather than waking up in the morning restored and rejuvenated, they are dragging themselves out of bed, facing another day feeling drained and exhausted. (1)

As you know, disrupted sleep can exert a severe toll on your emotional and physical health, interfering with mental abilities, productivity and performance - leaving you feeling stressed, cranky, depressed and drowsy. (2) Poor sleep patterns are linked to a growing list of serious health conditions, including obesity, heart disease, Type two diabetes, and even, premature deaths in older adults.

Sleep Problems Begin in Middle Age

Sleep researchers at the University of Pittsburgh have recently shown that alterations in normal sleep patterns actually begin in middle age. (3) Studying 110 volunteers between 20 to 59 years of age, they discovered that the quality and duration of sleep changed dramatically between the mid-20s and the mid-50s, with subjects going to bed and waking up earlier. The subjects also slept less, woke up more often during the night, and experienced fewer stages of deep sleep. (4)

According to study author, Dr. Julie Carrier, "Middle age is a turning point for sleep. Some sleep patterns have already changed significantly by the time an average adult reaches age 30." Dr. Carrier observed that these changes are most likely tied to gradual age-related changes in features of the biological clock. "We need to learn where the system breaks down. If we are able to find out what is causing the biological clock to change with age, we may be able to discover ways to overcome these changes and help get these people back on track."

Restoring Natural Sleep Cycles

Given the scope of the problem it's little wonder that the number of prescriptions for sleep aids has increased dramatically. According to data from IMS Health, 56,287,000 prescriptions were written last year for sleep medications like Ambien® and Lunesta®, a seven percent rise since 2007. My choice is to avoid prescribing fast-acting sleeping pills that tend to knock patients out and leave them with a hangover in the morning. I prefer, instead, to work with natural supplements combining nutrients that work together to gently promote a state of calm, initiate and support the natural process of falling asleep, and improve the overall quality of sleep to allow you to wake up feeling refreshed, energized and restored.

I most often recommend starting with two well-established supplements -- the neurohormone, melatonin, that is commonly used to treat jet lag and aid shift workers (e.g. police officers and nurses), and the amino acid, 5-HTP, which promotes serotonin production. More details on these in Natural Highs. I then add, if needed, a selection of traditional plant extracts, such as passionflower and valerian, that promote deep, restful sleep. Another favorite of mine is L-theanine, an amino acid derived from green tea that has been shown to aid in relaxing the mind and promoting a sense of calm.

Most recently I've been very impressed with a newly available version of a traditional Chinese herbal compound, Wulinshen, available in an aptly named formula, SleepCycle, along with the above-mentioned natural sleep enhancers. Wulinshen is known to help to re-synchronize the body's biological clock and sleep rhythms. It is rich in unique "deep-sleep" nutrients that help to relax the brain and promote a sense of calm to restore restful, recuperative sleep without next-day brain fog. It also reduces the time needed to fall to sleep, and, especially after seven to eight days of use, helps you to stay asleep longer. Wulinshen contains glutamic acid, gamma-aminobutyric acid (GABA, a calming amino acid, as well as a relaxing neurotransmitter) and glutamate decarboxylase, all of which are natural tranquilizers.

Many of my patients come to me after trying all the typical prescription and natural sleep products. They report that SleepCycle works even better than expected: they now just go to bed, fall asleep, and wake up feeling refreshed. It seems to gradually and steadily restore an optimal state of balance, promoting deep, restorative, recuperative sleep cycles over time.

In summary, rather than introducing foreign chemicals that can cause a host of their own problems, my preference is always to go for the natural products that work with the body's own chemistry.



1.Stoller, MK. Economic effects of insomnia. Clin Ther . 1994;16:873-97. Development Program. State-of-the-Science Conference.

2. Knipling R, Wang J. Revised estimates of the U.S. drowsy driver crash problem size based on general estimates system case reviews. Thirty-Ninth Annual Proceedings of the Association for the Advancement of Automotive Medicine . Des Plaines, IL: Association for the Advancement of Automotive Medicine; 1995:415-466.

3. E. J. W. Van Someren. "Circadian and sleep disturbances in the elderly." Experimental Gerontology, Volume 35, Issues 9-10, December 2000, Pages 1229-1237.

4. University Of Pittsburgh Medical Center. "Deterioration Of Sleep During Middle Age Related To Changes In The Biological Clock." ScienceDaily 25 June 1998.

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Vitamin C: Intravenous Use by Complementary and Alternative Medicine Practitioners and Adverse Effects

Posted By Administration, Monday, July 12, 2010
Updated: Friday, April 18, 2014


Background: Anecdotal information and case reports suggest that intravenously administered vitamin C is used by Complementary and Alternate Medicine (CAM) practitioners. The scale of such use in the U.S. and associated side effects are unknown. 

Methods and Findings: We surveyed attendees at annual CAM Conferences in 2006 and 2008, and determined sales of intravenous vitamin C by major U.S. manufacturers/distributors. We also queried practitioners for side effects, compiled published cases, and analyzed FDA’s Adverse Events Database. Of 199 survey respondents (out of 550), 172 practitioners administered IV vitamin C to 11,233 patients in 2006 and 8876 patients in 2008. Average dose was 28 grams every 4 days, with 22 total treatments per patient. Estimated yearly doses used (as 25g/50ml vials) were 318,539 in 2006 and 354,647 in 2008. Manufacturers’ yearly sales were 750,000 and 855,000 vials, respectively. Common reasons for treatment included infection, cancer, and fatigue. Of 9,328 patients for whom data is available, 101 had side effects, mostly minor, including lethargy/fatigue in 59 patients, change in mental status in 21 patients and vein irritation/phlebitis in 6 patients. Publications documented serious adverse events, including 2 deaths in patients known to be at risk for IV vitamin C. Due to confounding causes, the FDA Adverse Events Database was uninformative. Total numbers of patients treated in the US with high dose vitamin C cannot be accurately estimated from this study. 

Conclusions: High dose IV vitamin C is in unexpectedly wide use by CAM practitioners. Other than the known complications of IV vitamin C in those with renal impairment or glucose 6 phosphate dehydrogenase deficiency, high dose intravenous vitamin C appears to be remarkably safe. Physicians should inquire about IV vitamin C use in patients with cancer, chronic, untreatable, or intractable conditions and be observant of unexpected harm, drug interactions,orbenefit.



Among the most enduring of alternative medical treatments, vitamin C (ascorbic acid, ascorbate) is also one of the most popular. In 2007, it was the most widely sold single vitamin, with sales of 884 million dollars in the US1 [1]. Independent of its use to treat the deficiency disease scurvy, vitamin C has been used by non- mainstream physicians orally and parenterally for more than 60 years as a therapeutic agent [2–7]. Oral vitamin C is widely used by the public to prevent or treat infections, especially the common cold [8]. In one of its more controversial applications, gram doses of vitamin C were promoted by the two-time Nobel Laureate Linus Pauling as a cancer treatment agent [9,10]. Anecdotal evidence led us to posit that intravenous (IV) vitamin C is still used by Complementary and Alternative Medicine (CAM) practitioners to treat diverse conditions including infections, autoimmune diseases, cancer and illnesses of uncertain origin [11–13]. 

Despite its purported popularity, the extent of use of IV vitamin C is unknown. Its use in CAM has not been well publicized by practitioners and their patients, and is likely to be unrecognized by mainstream physicians. Benefits if any and especially side effects of such use may be unreported or under-reported. It is useful to know if high dose IV vitamin C therapy is widely used, and if so how and for what, so that conventional physicians can improve patient care by identifying any ill effects or drug interactions, and reporting benefit if any. 

New knowledge has elucidated possible mechanisms of action of IV vitamin C and for the first time made therapeutic effects biologically plausible [14]. It is now known that IV but not oral administration of vitamin C produces pharmacologic plasma concentrations of the vitamin [15,16]. Past studies used oral and/ or IV routes inconsistently, making such studies, in retrospect, flawed and difficult to interpret [17]. Recent in vitro experiments indicated that vitamin C only in pharmacologic concentrations killed cancer cells but not normal cells, and that the mechanism was via hydrogen peroxide formation [18]. In vivo animal data indicated that hydrogen peroxide was produced selectively in extracellular fluid around normal and tumor tissues by pharma- cologic vitamin C concentrations [19,20]. At these concentrations, vitamin C slowed tumor growth [20,21]. Pharmacologic vitamin C concentrations produced in animals by parenteral administration were reproduced in patients in a recent phase I clinical trial [16]. 

Because of the new interest in IV vitamin C, coupled to need to characterize use and uncover side effects, we surveyed CAM practitioners anonymously. We also searched for side effects of IV vitamin C administration in the published medical literature and in the Food and Drug Administration (FDA) adverse events database, and estimated sales volumes of IV vitamin C preparations. 

Our study obtained quantitative information that substantiated previous anecdotal reports. Despite unexpected wide use, we found side effects of vitamin C were surprisingly few when patients were properly screened. The findings in this paper will alert conventional practitioners about unrecognized wide use of IV vitamin C, will remind them to query patients about such use, and may help to uncover either unexpected adverse events or benefit and spur further research in this area. 



Survey Methods 

The study was reviewed by the Human Subjects Committee/ Institutional Review Board at the University of Kansas Medical Center. The survey was categorized as an exempt study. It contained no personal identifiers; therefore informed consent was not necessary under exempt status and was not obtained. Survey forms were distributed to practitioners attending a conference on CAM in 2006 and 2008. Participants were requested to return completed survey forms before the end of each conference. Participants were asked whether they used high dose IV vitamin C during the preceding 12 months, and if so, to detail its use by answering specific questions in the survey form (see Survey S1 for the survey form used). It was not possible to identify the respondent from the survey form or survey data. The same form was used in both years, with an additional line on the 2008 form inquiring whether the respondent had also responded in 2006 (See Survey S1). 

Vitamin C doses sold 

The major manufacturers/importers in the US of vitamin C preparations that can be administered IV were contacted by telephone. Data on annual sales of vitamin C in the US were obtained with the understanding that the names and sales figures of individual companies would not be linked nor made public. 

Side effects of high dose IV vitamin C

We searched the Adverse Events Reporting System, a database of drug side effects maintained by the Food and Drug Administration (FDA). Data from 20 consecutive quarters available from 2004–2008 were queried. We also searched for side effects in publications on therapeutic use of high dose IV vitamin C. We searched Medline, Web of Science (ISI Thompson) and Scopus databases for papers in English that reported IV vitamin C administration in humans. Several different search terms and possible variants of each search term were used to capture the maximum number of papers. Papers reporting oral vitamin C treatment only, or those using IV doses of 1g or less, were excluded. Because vitamin C is sometimes administered IV in patients undergoing hemodialysis, there are many published studies in this area. A separate search was conducted for papers reporting these to ensure that these were excluded from our analysis. IV administered vitamin C is also used to study the acute effects of antioxidants or of vitamin C itself on metabolism and physiology, particularly on cardiovascular and endothelial reac- tivity. This does not constitute a therapeutic use of vitamin C. Hence publications reporting these were identified and removed from the search results. Separately, we searched the same databases for specific reports of side effects of IV administered vitamin C and followed up references and cited papers. From papers so collected, we manually eliminated duplicate citations and those that did not meet the above criteria. From the remaining reports, adverse reactions attributable to IV adminis- tered vitamin C were noted. 


Survey response 

We distributed 300 survey forms in 2006 to attendees at their annual CAM conference. 106 forms were returned, a response rate of 35%. In 2008, 250 survey forms were distributed and 93 completed forms were returned, a response rate of 37%. Of the 2008 respondents, 22 (24%) had previously responded in 2006. An unknown number of conference attendees were not practitioners but spouses, researchers or industry representatives who did not return survey forms, reducing response rates. 

Vitamin C usage 

Of 199 total respondents for 2006 and 2008: 172 practitioners administered vitamin C; 27 did not use IV Vitamin C; 48 practitioners treated more than 100 patients each per year; and 5 treated more than 1000 patients each per year (Figure 1A, B). 11,233 patients received IV vitamin C in 2006 and 8876 in 2008 (figure 1A, B). On average, each patient received 22 treatments (Table 1). Treatments occurred at a mean of once every 4 days, each at a mean dose of 28 grams (Table 1). Doses used were as low as 1gram or as high as 200grams, with a similar wide range for each of the parameters queried. Based on dosing vials of 25g/ 50ml, estimated total yearly dosing vials administered were 318,539 in 2006 and 354,647 in 2008. Estimated total number of dosing vials sold was independently obtained from the major manufacturers of vitamin C in the U.S. Total dosing vials of IV vitamin C sold in the United States were approximately 750,000 in 2006 and 855,000 in 2008 (Table 1). 

Seventy seven percent of respondents reported the numbers of patients treated for broad indications, labeled as infection (44%), cancer (19%) or other conditions (37%) (Table 2). Numbers of practitioners who listed specific indications for treatment are shown in figure 2. Practitioners listed fatigue as the most common specific single indication for treatment in 2006, and breast cancer in 2008. There were a large number of indications for which less than four practitioners used high dose IV vitamin C (Table S1). 

Adverse effects 

Adverse events reported by survey respondents were minor (Table 3). No side effects were reported for 9227 patients while 59 were reported to have lethargy or fatigue. A single practitioner listed change in mental status in 10% of his patients (20 patients) but provided no details. One patient with pre existing renal impairment and cancer metastases to kidneys was reported to have developed unconfirmed renal failure. Some practitioners reported side effects without reporting patient numbers. The most common of these side effects were lethargy or fatigue (reported by 27 practitioners), vein irritation (by 9 practitioners), and nausea and vomiting (by 9 practitioners). Other reported side effects are listed in table 3. Less commonly reported adverse effects are listed in Table S2. 

Data obtained from the FDA Adverse Events Reporting System database for 20 consecutive quarters indicated that 77 patients treated with 0.2–1.0 gram doses of IV vitamin C had reported adverse events (Table 4). However, all patients either had serious or life-threatening systemic illnesses, and/or were receiving many potentially toxic drugs (i.e. cancer therapeutics) in addition to IV vitamin C (for details, see Table S3). Some individual patients appear to have been reported multiple times (see Table S3). In comparison to CAM practitioners, the dose of vitamin C administered was very low (1 gram or less). In no case could we exclude multiple confounding factors as the cause of the reported adverse effects (Table 4). Whether vitamin C caused or contributed to these side effects cannot be determined from the available data. 

Through searching published literature (see methods for details), 187 papers were found on the use of high dose IV vitamin C, including papers that reported side effects. There were three cases of renal failure, all in patients with pre existing renal impairment [22,23], [24]. Two patients with glucose 6 phosphate dehydroge- nase deficiency developed hemolysis [25,26] (Table 5). 

Practitioner Demographics 

86% of practitioners were physicians (Table 6) and most patients were treated at for-profit centers. Some practitioners did not provide requested demographics data. Therefore, the numbers given in this table do not tally with the total number of survey respondents. (For detailed demographic information, see Table S4).

Table 1. Details of high dose IV vitamin C use by survey respondents for the years 2006 and 2008. 



                                                                                                                      Mean Median Range

Dose (g/treatment)                                                                 28    31       1-200

Number of treatments per patient                                                19    16       1-80

Number treated by one practitioner                                              121    40       1-1150

Duration of treatments (min)                                                      105    90       2-1440

Frequency of treatments (once every so many days)                           4     3.5       1-7

Lowest dose (g/treatment)                                                         12    9       1-60

Highest dose (g/treatment)                                                         79    75       5-200

Infusion rate (g/min)                                                                0.89    0.5     0.03-25

Total number of vials of vitamin C used (25g/50ml) (Calculated from survey data)       318,539

Total number of vials of vitamin C sold by companies in the US (25g/50 ml)               750,000


                                                                                                                         Mean Median Range


Dose (g/treatment)                                                                                          28    50       1-200

Number of treatments per patient                                       24    16       1-80                

Number treated by one practitioner                                                               112    40       1-3000

Duration of treatments (min)                                                                         81    90       1-900

Frequency of treatments (once every so many days)                                      4      2       1-7

Lowest dose (g/treatment)                                                                             17    15       1-75


Highest dose (g/treatment)                                                                            87    95       20-200

Infusion rate (g/min)                                                                                      0.525  0.5    0.028-2.5        

Total number of vials of vitamin C used (25g/50ml) (Calculated from survey data)     354,647 

Total number of vials of vitamin C sold by companies in the US (25g/50 ml)          855,000 

Vitamin C is supplied in 50 ml bottles containing 25 grams. Estimated total number of doses (bottles) used each year was calculated as the cumulative sum of each practitioners’ number of patients that practitioners’ average dose in bottles that practitioner’s average number of doses per patient. doi:10.1371/journal.pone.0011414.t001



Table 2.Indications for treatment with high dose IV vitamin C. 





Year                                                                                                        2006     2008

Total number of patients treated                                                          11233    8876


Number of patients with data available                             9481      5928

Number of patients with          Infection                                  4587      2264

                              Cancer                              1379     1509

                              Other Conditions                   3515     2155






Some respondents did not list the number of patients treated for each of the 




conditions for which they used intravenous vitamin C treatment. Therefore, the 




data do not provide indications for treatment for all patients who received IV 




vitamin C. 








The data here show that 11,233 and 8876 patients received IV vitamin C over two periods of one year each, with a mean number of infusions per patient of 19–24 and a mean dose of approximately 28 grams per patient. We estimate that survey respondents used approximately 318,539 and 354,647 dosing units of vitamin C each year. These numbers account for less than half of the doses of vitamin C doses sold within the United States for the matching year. Considered together, these data indicate that use of IV vitamin C was both substantial and probably underestimated. This is one of the first papers to document previously unrecognized and widespread use of a CAM agent administered IV. To our knowledge, only two other CAM therapies are used IV. The first, chelation therapy, is also used in standard medical practice [27]. The second, an IV vitamin and mineral mixture termed the Myer’s cocktail, has variable components, has had little formal investigation, and contains less than 5 grams of vitamin C [28,29]. Further, there have been few surveys of CAM practitioners, as opposed to surveys of patients. There were minimal adverse effects reported, which was also the case in the published literature. Exceptions were for patients with pre-existing renal insufficiency/failure or glucose 6-phosphate dehydrogenase (G6PD) deficiency, both known to predispose to vitamin C toxicity [30]. Adverse events reported to the FDA could not be interpreted due to confounding factors. 

Table 3. Adverse events reported with IV vitamin C use in the survey for the years 2006 and 2008.

                                                                                                              # of Patients


Complication                                                                                         2006   2008 

None Described                                                   5349   3878 

Lethargy/Fatigue                                                 10       49 

Local Vein Irritation                                                3        - 

Phlebitis                                                           3        - 

Kidney Stone (oxalate)                                             -         1 

Kidney Stone (urate)                                               -         1 

Kidney Stone (unspecified)                                         2         - 

Hemolysis                                                         2         - 

Elevated Blood Glucose                                            2         - 

Muscle Cramps                                                                 1         - 

Headache                                                         1        - 

Change in Mental Status                                           1       20 

Nausea/Vomiting                                                  1       - 

Flu Like Syndrome                                                 1        - 

Renal Failure                                                                   -         1* 

Syncope                                                                         -         1 

Pain at Tumor                                                     -         1 

No Data                                                                        5857      4924 

Data included in the table represent only those practitioners who reported exact patient numbers. *Described as ‘‘not confirmed (possible). Patient had partial renal failure and cancer metastases to kidneys.’’ Data on practitioners who reported adverse events but did not report the number of patients affected are detailed below as: side effect (with the number of practitioners who reported each side effect in parenthesis). For the year 2006: lethargy/fatigue (9), local vein irritation (3), nausea/vomiting (2), hypoglycemia (2), allergy (2), phlebitis (1), cellulitis (1), hematuria (1), dry mouth (1), Herxheimer reaction (1), localized thrombosis (1), and syncope (1). For the year 2008: lethargy/fatigue (9), nausea/vomiting (6), local vein irritation (4), headache (3), phlebitis (3), heartburn (1), dizziness (1), venosclerosis (1), mild palpitation (1), and cold (1), dizziness (1), ‘‘initiation of mem occasionally’’ (1), and other (1). doi:10.1371/journal.pone.0011414.t003

Soon after its discovery and synthesis in 1932, parenteral vitamin C was shown to significantly decrease polio virus infections in primates [31,32]. Although these findings were not repeatable [33,34], one practitioner treated thousands of patients with parenteral vitamin C, primarily for infections, and popular- ized its use [2,3,5]. Such reports probably were a basis for continued use of parenteral vitamin C by other CAM practitioners [6,7,35]. Independently, others postulated that vitamin C could be useful in cancer treatment by enhancing or strengthening collagen and intercellular matrix synthesis and thereby decreasing metas- tases [36,37]. Ewan Cameron, joined by Nobelist Linus Pauling, reported in retrospective case series that oral and IV vitamin C might benefit patients with advanced cancers [9,10]. Placebo- controlled double blinded clinical trials at the Mayo Clinic showed no efficacy [38–40] but CAM practitioners continued to use IV vitamin C [11,13,35], consistent with our survey results. Pharmacokinetics evidence [15,41,42] now reveals that the exclusively oral vitamin C doses used in the Mayo studies would have produced peak plasma concentrations of approximately 0.2 mM, while the same dose given IV would produce peak plasma concentrations approximately 25 fold higher [15].  

Table 4.Adverse effects reported to the Food and Drug Administration (FDA) in patients treated with IV vitamin C. 


Year      Number of Cases reported        Dose Range(g/day)        Can confounders be eliminated? 

2004       15                                              0.5–1                               No 

2005       7                                                0.25–1                             No 

2006      11                                               0.2–1                               No 

2007      11                                              Not Given                         No 

2008      33                                               0.5–1                               No 


When the vitamin C dose was provided as ml, the dose was converted to mg on the basis that vitamin C is supplied as 0.5gram/ml solution. Some practitioners did not mention the dose of vitamin C used. The format of the FDA adverse events database did not permit identification of specific patients, so that the same patient may have been reported multiple times in the same quarter or in several quarters, inflating the number of patients with adverse events. doi:10.1371/journal.pone.0011414.t004 



Pharmacologic doses of vitamin C given IV may produce drug effects in many body tissues, mediated by hydrogen peroxide formation in extracellular fluid but not blood [18–20]. Emerging clinical data are consistent with plausibility [43] and safety [16], but whether there is benefit or harm in humans can only be addressed by rigorous clinical trials. 

IV vitamin C administered in gram doses can cause serious side effects in some patients. A metabolic end-product of vitamin C metabolism is oxalate, and oxalate nephropathy has been reported in patients with renal impairment given gram doses of IV vitamin C [22–24]. Prolonged treatment with vitamin C increases plasma oxalate concentrations in patients with renal failure [44] and results in increased urinary oxalate in patients receiving total parenteral nutrition [45], although in these patient groups the consequences of hyperoxalemia are unknown. Patients with glucose 6-phosphate dehydrogenase deficiency can develop intravascular hemolysis when gram doses of vitamin C are given IV [25,26]. Vitamin C, even with oral dosing, might induce hemolysis in patients with Paroxysmal Nocturnal Hemoglobinuria [46,47]. A recent phase one study of high dose IV vitamin C in patients with advanced cancer did not find any serious side effects [16]. Exclusion criteria for the phase I study included renal failure and glucose-6-phosphate dehydrogenase deficiency. Recently, a study in mice reported decreased efficacy of cancer chemother- apeutic agents with parenteral dehydroascorbic acid, a metabolite of vitamin C [48]. Dehydroascorbic acid cannot be detected in human blood or tissues, is not commercially available for parenteral use nor used by CAM practitioners, is toxic at high concentrations [49,50], and should not be administered parenterally in humans. 

No definitive serious adverse events were reported by survey respondents. Despite the anonymity of the survey, practitioners may have been reluctant to describe adverse events. Whether IV vitamin C is safe for general use remains to be determined. Because of the possibility of unrecognized side effects or of drug interactions, practitioners should enquire whether their patients, especially those with chronic, intractable or difficult to treat conditions, are receiving high dose IV vitamin C treatment elsewhere. Physicians should be alert to potential interactions of high dose vitamin C not only with conventional medicines but also with CAM treatments. An example is the case of exacerbated, severe cyanide poisoning in a patient on concurrent treatment with high dose oral vitamin C and Amygdalin (laetrile, a metabolic product of which is cyanide) [51]. 

Our study has limitations that, when considered together, may underestimate use of IV vitamin C. Because our survey was distributed to participants in a CAM conference, the survey excluded the vast majority of CAM practitioners. Respondents who filled in the survey form did so from memory without access to records, so that the information obtained can only be considered approximate. The format of the survey questions may have inadvertently resulted in underestimating vitamin C use, because the survey questions used ranges, for simplicity. For example, the highest value listed for numbers of patients treated in a calendar year was ‘‘>40’’. If practitioners did not specify precise numbers as requested in subsequent questions, 40 was used as the number of patients treated, although the true number may have been higher. That there was only 24% overlap between survey respondents in 2006 and 2008 provides additional evidence that community use of IV vitamin C was underestimated. Data concerning industry sales of IV ascorbate only give approxima- tions of use. On one hand, because not all units sold would have been used, use may be overestimated. Conversely, other smaller companies and compounding pharmacies may supply parenteral vitamin C but were not included in the survey. Therefore, the total number of vials sold may also be underestimated. The exact number of doses of parenteral vitamin C used in the US per year remains unknown. The survey response rate of approx 35% suggests we underestimated use, and perhaps adverse events. A reduced response rate may have occurred because some conference attendees were not practitioners and therefore did not return survey forms. Because of these uncertainties, the number of US patients treated with IV vitamin C cannot be accurately estimated from survey data. Since a primary aim of the survey was to determine if IV administered vitamin C is in use, and not a census of patients treated, the response rate does not detract from the value of the data. 

Data obtained on adverse effects from PUBMED and the FDA also have limitations. Physicians may have not reported compli- cations because they were not recognized, or were delayed, or were not attributed to vitamin C. Most practitioners do not report or publish adverse events. There may be as yet unknown adverse effects or interactions of IV ascorbate with other drugs. Side effects reported to FDA are difficult to interpret because of confounding factors. All reported patients received other potentially toxic drugs and/or had other diagnoses that may have been responsible for the reported adverse effects (see Table S3). Because of the FDA adverse events format, the same patient was likely to have been reported multiple times. Because of the low doses of IV vitamin C in the FDA dataset, it is highly unlikely that any of the reported adverse effects were due to the vitamin. Despite this, and because the information available in the FDA database is limited, it is not possible to accurately determine whether vitamin C caused or contributed to the reported side effects. 

IV vitamin C is already in wide use, and physicians should know that their patients may seek IV vitamin C treatment in addition to conventional therapies. Beneficial effects of intravenous vitamin C on the disease conditions for which it is used are unproven, but side effects appear to be minor. Physicians should be cognizant of potential adverse or other unexpected effects, and of unrecognized interactions with drugs used in conventional and alternative medicine. CAM practitioners have an obligation to screen patients and should not administer high dose IV vitamin C to patients with pre existing renal disease, renal insufficiency or renal failure; glucose 6-phosphate dehydrogenase deficiency; a history of oxalate nephrolithiasis; or paroxysmal nocturnal hemoglobinuria. Based on emerging evidence, vitamin C in pharmacologic concentrations appears to be a pro-drug for delivery of hydrogen peroxide to the extravascular space. High dose IV vitamin C appears to have a positive safety profile, favorable pharmacology, evidence for mechanism of action, some anti-cancer effects in vitro and in animals, and widespread use outside conventional medicine with minimal harm, but without any proven clinical benefit. 

Supporting Information 

Table S1 

Found at: doi:10.1371/journal.pone.0011414.s001 (0.18 MB DOC) 

Table S2 

Found at: doi:10.1371/journal.pone.0011414.s002 (0.05 MB DOC) 

Table S3 

Found at: doi:10.1371/journal.pone.0011414.s003 (0.17 MB DOC) 

Table S4 

Found at: doi:10.1371/journal.pone.0011414.s004 (0.04 MB DOC) 

Survey S1 Survey Form 

Found at: doi:10.1371/journal.pone.0011414.s005 (0.05 MB DOC) 


We thank CAM practitioners for their cooperation in completing the surveys, and Dr. Jill Norris, University of Colorado Health Sciences Center, for advice on preparing the survey. 

Author Contributions 

Conceived and designed the experiments: SJP AYS QC MGE JD ML. Performed the experiments: SJP AYS QC MGE JD ML. Analyzed the data: SJP AYS QC MGE JD ML. Contributed reagents/materials/analysis tools: SJP AYS QC MGE JD ML. Wrote the paper: SJP AYS QC MGE JD ML.


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31. Jungeblut CW (1935) Inactivation of poliomyelitis virus in vitro by crystalline vitamin C (ascorbic acid). Journal of Experimental Medicine 62: 517–21.

32. Jungebl ut CW ( 1937) Further observations on vi tami n C therapy in experimental poliomyelitis. Journal of Experimental Medicine 66: 459–77. 

33. Sabin AB (1939) Vitamin C in relation to experimental poliomyelitis. Journal of Experimental Medicine 69: 507–16. 

34. Jungeblut CW (1939) A further contribut ion to vitamin C therapy in experimental poliomyelitis. Journal of Experimental Medicine 70: 315–32. 

35. Riordan HD, Jackson JA, Schultz M (1990) Case study: high-dose intravenous vitamin C in the treatment of a patient with adenocarcinoma of the kidney. J Orthomolecular Med 5: 5–7. 

36. McCormick WJ (1954) Cancer: the preconditioning factor in pathogenesis; a new etiologic approach. Arch Pediatr 71: 313–22. 

37. Cameron E, Rotman D (1972) Ascorbic acid, cell proliferation, and cancer. Lancet 1: 542. 

38. Moertel CG, Fleming TR, Creagan ET, Rubin J, O’Connell MJ, Ames MM (1985) High-dose vitamin C versus placebo in the treatment of patients with advanced cancer who have had no prior chemotherapy. A randomized double- blind comparison. N Engl J Med 312: 137–41. 

39. Creagan ET, Moertel CG, O’Fallon JR, Schutt AJ, O’Connell MJ, Rubin J, et al. (1979) Failure of high-dose vitamin C (ascorbic acid) therapy to benefit patients with advanced cancer. A controlled trial. N Engl J Med 301: 687–90. 

40. Wittes RE (1985) Vitamin C and cancer. N Engl J Med 312: 178–79. 

41. Levi ne M, Conry- Cant i l ena C, Wang Y, Wel ch RW, Washko PW, Dhariwal KR, et al. (1996) Vitamin C pharmacokinetics in healthy volunteers: evidence for a Recommended Dietary Allowance. Proc Natl Acad Sci U S A 93: 3704–9. 

42. Levine M, Wang Y, Padayatty SJ, Morrow J (2001) A new recommended dietary allowance of vitamin C for healthy young women. Proc Natl Acad Sci U S A 98: 9842–46. 

43. Padayatty SJ, Levine M (2006) Vitamins C and E and the prevention of preeclampsia. N Engl J Med 355: 1065. 

44. Canavese C, Petrarulo M, Massarenti P, Berutti S, Fenoglio R, Pauletto D, et al. (2005) Long-term, low-dose, intravenous vitamin C leads to plasma calcium oxalate supersaturation in hemodialysis patients. Am J Kidney Dis 45: 540–549. 

45. Pena dl V, Lieske JC, Milliner D, Gonyea J, Kelly DG (2004) Urinary oxalate excretion increases in home parenteral nutrition patients on a higher intravenous ascorbic acid dose. JPEN J Parenter Enteral Nutr 28: 435–38. 

46. Iwamoto N, Kawaguchi T, Horikawa K, Nagakura S, Hidaka M, Kagimoto T, et al. (1994) Haemolysis induced by ascorbic acid in paroxysmal nocturnal haemoglobinuria. Lancet 343: 357. 

47. Iwamoto N, Nakakuma H, Ota N, Shimokado H, Takatsuki K (1994) Ascorbic acid-induced hemolysis of paroxysmal nocturnal hemoglobinuria erythrocytes. Am J Hematol 47: 337–38. 

48. Heaney ML, Gardner JR, Karasavvas N, Golde DW, Scheinberg DA, Smith EA, et al. (2008) Vitamin C antagonizes the cytotoxic effects of antineoplastic drugs. Cancer Res 68: 8031–38. 

49. Pat t erson JW ( 1950) The di abet ogeni c effect of dehydroascorbic and dehydroisoascorbic acids. J Biol Chem 183: 81–88. 

50. Patterson JW (1951) Course of diabetes and development of cataracts after injecting dehydroascorbic acid and related substances. Am J Physiol 165: 61–65. 

51. Bromley J, Hughes BG, Leong DC, Buckley NA (2005) Life-threatening interaction between complementary medicines: cyanide toxicity following ingestion of amygdalin and vitamin C. Ann Pharmacother 39: 1566–69.

Source: Padayatty SJ, Sun AY, Chen Q, Espey MG, Drisko J, et al. (2010) Vitamin C: Intravenous Use by Complementary and Alternative Medicine Practitioners and Adverse Effects. PLoS ONE 5(7): e11414. doi:10.1371/journal.pone.0011414. Editor:Joel Joseph Gagnier, University of Michigan, Canada. ReceivedFebruary 23, 2010;AcceptedMay 30, 2010;PublishedJuly 7, 2010. 

Tags:  vitamin C 

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Coenzyme Q10 and the Heart

Posted By Administration, Wednesday, July 7, 2010
Updated: Friday, April 18, 2014


Zinaby Zina Kroner, DO

CoQ10 has been considered for prevention and treatment of cardiovascular disease related to atherosclerosis, hypertension, diabetes and other common risk factors. LDL (“bad cholesterol”) in the walls of arteries can be oxidatively damaged and that may be an initiating event leading to atherosclerosis. In these cases, the antioxidant function of CoQ10 might be beneficial. There are other properties of CoQ10 that are of interest, such as its ability to decrease the amount of a specific substance on the surface of cells that can collect on the blood vessel walls (1).

An analysis of available research in 2003 found conflicting results. Some improvement in cardiac function was observed in some studies, but not confirmed in others (4). 

CoQ10 is considered as a possible treatment for cardiomyopathy, which is an abnormality or disease of the cardiac muscle. Improvements in cardiac output have been found in some small studies. It has also been shown to help congestive heart failure as the result of coronary heart disease in other small studies. Again, there is a need for more large-scale clinical trials (1, 3).

Levels of CoQ10 have been considered as an independent predictor for outcome in patients with chronic heart failure. Those with lower levels have a higher risk of death. In one recent study, the correlation was strong enough for investigators to call for more interventional studies using CoQ10 to treat heart failure (4). 

This same pattern repeats for almost all types of cardiovascular disease and treatment. From the treatment of angina (lack of blood supply to the heart muscle), to high blood pressure and damage of the lining of the blood vessels, there is some evidence of benefit from CoQ10 and a need for more studies (1).  

I make sure that my patients' coq10 levels are assessed and they are treated accordingly.



1. Higdon, J. Coenzyme Q10. Micronutrient Information Center. Linus Pauling Institute. 2/2003. Updated 2/2007. (Accessed 5/27/2010)

2. Shekelle P, Morton S, Hardy M. Effect of Supplemental Antioxidants Vitamin C, Vitamin E, and Coenzyme Q10 for the Prevention and Treatment of Cardiovascular Disease. Summary, Evidence Report/Technology Assessment: Number 83. AHRQ Publication Number 03-E042, June 2003. Agency for Healthcare Research and Quality, Rockville, MD.

3. Dallner, G, Stocker, R. Coenzyme Q10. Encyclopedia of dietary supplements, ed Paul M. Coates.  Marcel Dekker, New York. 2005.

4. Molyneux, SL, Florkowski, CM, George, PM, et al. Coenzyme Q10: An Independent Predictor of Mortality in Chronic Heart Failure. J. Am. Coll. Cardiol. 2008;52;1435-1441.

Tags:  coenzyme Q10  heart 

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Acupuncture for Ovulation Disorders and PCOS

Posted By Administration, Friday, July 2, 2010
Updated: Friday, April 18, 2014


by Fiona McCulloch, ND


Polycystic ovarian syndrome is the number one reproductive disease in women.   This disease disrupts normal ovulatory cycles which can result in heartbreaking infertility for millions of women.  Known hormonal changes in PCOS include excess androgens (ie: testosterone), and insulin resistance.  Most thought now is leaning towards insulin resistance being the primary cause of PCOS, with genetic factors playing a role, but once the cycle of anovulation begins it feeds back on itself, causing the condition to remain in a vicious cycle.  Women with PCOS have not only insulin resistance, but also have neuroendocrine imbalances, resulting in elevated LH (lutenizing hormone) levels.  Having a high LH to FSH ratio is one of the hallmarks of polycystic ovarian syndrome or persistent anovulation.  In response to a combination of high LH and insulin resistance, the follicles in the ovary will begin to secrete too many male hormones (androgens) which then inhibit the hormonal pathways that are needed to stimulate ovulation.


Various medications are traditionally used to induce ovulation in women with PCOS.  A growing body of evidence now exists indicating that low-frequency electroacupuncture is as effective as commonly used medications in inducing ovulation.  Furthermore, this form of acupuncture can benefit many of the hormonal imbalances seen in polycystic ovarian syndrome.  Thousands of women worldwide use acupuncture therapy for PCOS and so I’d like to discuss how it works, and why it is so beneficial to induce ovulation.

General principles of how electroacupuncture stimulates the ovaries through the nervous system

Electroacupuncture has been found to profoundly effect the reproductive organs, through mechanisms in the sympathetic nervous system, endocrine system, and neuroendocrine system.  When needles are inserted into certain points and stimulated in a specific manner, this produces a neurological reflex transmitted to the organ correlated with that nerve pathway.  For example, needles inserted into the leg muscles below the knee, lower back, or abdomen in specific regions cause a response which measurably affects the ovary.  In addition, the nervous system will transmit a signal to the brain, and the brain then emits a response which affects the organ from a central mechanism.  These effects have been investigated through measurements of hormones, neuropeptides, and circulatory changes on both animals and humans receiving this specific type of electroacupuncture.

Nervous system alterations in PCOS

Evidence indicates that women with pcos have abnormal circulating levels of a neurohormone called β-endorphin.  β-endorphin is known to increase insulin production and reduce insulin excretion by the liver, which is very much implicated in PCOS.   It has also been found that women with PCOS have unusually high amounts of sympathetic nerve fibres in their ovaries.  These nerve fibres cause unusual stimulation of the ovary by the sympathetic nervous system (the part of the nervous system associated with “flight or fight” responses in the body, among other processes).  Stimulation of these nerve fibres can cause the ovaries to produce androgens, which then impair normal ovulation.  Women with PCOS have also been found to have high amounts of nerve growth factors in their ovaries, something which is associated with high levels of sympathetic nervous system activity.   Disturbances in central and peripheral β-endorphin release, high androgens, insulin resistance, abdominal obesity, and cardiovascular disease are associated with increased sympathetic nervous system activity, and all of these are also associated with the pathology of PCOS.  In a recent study by Elizabet Stener-Vitorin in Sweden, direct intraneural testing found a strong correlation between levels of sympathetic nervous system activity and testosterone levels in women with PCOS.  Those who had the highest amounts of sympathetic nervous system activity were found to have the highest testosterone levels and the most severe PCOS conditions.

What evidence exists for acupuncture inducing ovulation?

Several studies exist on low frequency electroacupuncture and ovulation induction.  In one trial, the effect of a series of 14 electroacupuncture treatments on 24 anovulatory women with pcos was investigated.  In 38% of these women, regular ovulation was induced.   Three months after the last treatment, LH/FSH ratios and testosterone levels were significantly decreased, a sign of improvement in PCOS pathology.   In another study done on a group of women given human menopausal gonadotrophin (a commonly used drug in the treatment of infertility), acupuncture was compared to hCG injections in order to assess its effect on ovulation.  Traditionally hCG is given to stimulate ovulation during medicated cycles at fertility clinics.  It was found that a single acupuncture treatment induced ovulation as effectively as the as the hCG injection and reduced the incidence of ovarian hyperstimulation syndrome, a painful side effect of medicated cycles.  Other studies have also indicated enhanced ovarian response when acupuncture is added to medicated cycles.  Female rats with PCOS induced by chronic exposure to DHT (a form of testosterone) were given low frequency electroacupuncture and physical exercise.  The treatment increased the amount of healthy follicles in the ovaries,  and significantly normalized cycles.

Effects of electroacupuncture on nervous system changes in PCOS

It has also been found that electro-acupuncture can regulate parts of the central nervous system related to dysfunction in PCOS.  Specifically, beneficial effects on neurohormones such as GnRH(Gonadotropin releasing hormone) and androgen receptor proteins, indicate that electro-acupuncture significantly benefits the hypothalamic-pituitary-ovarian axis and through this can help to restore normal cycling.  Electroacupuncture was also found in 3 recent studies to increase ovarian blood flow through effects on sympathetic nervous system pathways.  In addition, it has been found in two studies to reduce high peripheral circulating β-endorphins in women with PCOS, and thereby improve insulin resistance.   As sympathetic nerve activity appears to contribute to the development and maintenance of PCOS, the beneficial effects of electroacupuncture, and also exercise, may be mediated by nervous system modulation to the ovaries.

Electro-acupuncture appears to work through multiple pathways to disrupt the “vicious cycle” of PCOS.  Even though much more research needs to be done to determine all of the mechanisms involved, its safety and low incidence of side effects makes it an excellent therapy to stimulate ovulation naturally for the many women who suffer with this disease.


Andersson, S., Lundeberg, T., 1995. Acupuncture — from empiricism to science:functional background to acupuncture effects in pain and disease. Med. Hypotheses 45, 271–281.


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Carmina, E., Ditkoff, E.C., Malizia, G., Vijod, A.G., Janni, A., Lobo, R.A., 1992. Increased circulating levels of immunoreactive beta-endorphin in polycystic ovary syndrome is not caused by increased pituitary secretion. Am. J. Obstet. Gynecol. 167,

Chen, B.Y., Yu, J., 1991. Relationship between blood radioimmunoreactive beta-endorphin and hand skin temperature during the electro-acupuncture induction of ovulation. Acupunct. Electrother.

Lobo, R.A., Granger, L. R., Paul, W.L., Goebelsmann, U., Mishell Jr., D.R., 1983. Psychological stress and increases in urinary norepinephrine metabolites, platelet serotonin, and adrenal androgens in women with polycystic ovary syndrome. Am. J. Obstet. Gynecol. 145, 496–503.

Feng, Y., Johansson, J., Shao, R., Manneras, L., Fernandez-Rodriguez, J., Billig, H., Stener-Victorin, E., 2009. Hypothalamic neuroendocrine functions in rats with dihydrotestosterone-induced polycystic ovary syndrome: effects of low-frequency electroacupuncture. PLoS ONE 4, e6638. produces skeletal muscle vasodilation following antidromic stimulation of unmyelinated afferents in the dorsal root in rats. Neurosci. Lett. 283, 137–140.

Jin, C.L., Tohya, K., Kuribayashi, K., Kimura, M., Hirao, Y.H., 2009. Increased oocyte production after acupuncture treatment during superovulation process in mice. J. of Reprod. & Conception 20, 35–44.

Manneras, L., Cajander, S., Lonn, M., Stener-Victorin, E., 2009. Acupuncture and exercise restore adipose tissue expression of sympathetic markers and improve ovarian morphology in rats with dihydrotestosterone-induced PCOS. Am. J. Physiol. Regul. Integr. Comp. Physiol. 296, R1124–R1131.

Stener-Victorin, E., Wu, X., Effects and mechanisms of acupuncture in the reproductive system, Auton. Neurosci.(2010)

Stener-Victorin, E., Lindholm, C., 2004. Immunity and beta-endorphin concentrations in hypothalamus and plasma in rats with steroid-induced polycystic ovaries: effect of low-frequency electroacupuncture. Biol. Reprod. 70, 329–333.

Stener-Victorin, E., Waldenstrom, U., Tagnfors, U., Lundeberg, T., Lindstedt, G., Janson, P.O., 2006. Effects of electro-acupuncture on anovulation in women with polycystic ovary syndrome. Acta Obstet. Gynecol. Scand.

Stener-Victorin, E., Lundeberg, T., Waldenstrom, U., Manni, L., Aloe, L., Gunnarsson, S., Janson, P.O., 2000a. Effects of electro-acupuncture on nerve growth factor and ovarian morphology in rats with experimentally induced polycystic ovaries. Biol. Reprod. 63, 1497–1503.

Stener-Victorin, E., Lundeberg, T., Waldenstrom, U., Bileviciute-Ljungar, I., Janson, P.O., 2001. Effects of electro-acupuncture on corticotropin-releasing factor in rats with experimentally-induced polycystic ovaries. Neuropeptides 35, 227–231.

Stener-Victorin, E., Kobayashi, R., Kurosawa, M., 2003a. Ovarian blood flow responses to electro-acupuncture stimulation at different frequencies and intensities in anaesthetized rats. Auton. Neurosci.: Basic and Clin. 108, 50–56.

Stener-Victorin, E., Lundeberg, T., Cajander, S., Aloe, L., Manni, L., Waldenstrom, U., Janson, P.O., 2003b. Steroid-induced polycystic ovaries in rats: effect of electro- acupuncture on concentrations of endothelin-1 and nerve growth factor (NGF), and expression of NGF mRNA in the ovaries, the adrenal glands, and the central nervous system. Reprod. Biol. Endocrinol. 1, 33.

Stener-Victorin, E., Fujisawa, S., Kurosawa, M., 2006. Ovarian blood flow responses to electroacupuncture stimulation depend on estrous cycle and on site and frequency of stimulation in anesthetized rats. J. Appl. Physiol. 101, 84–91.

Stener-Victorin, E., Jedel, E., Manneras, L., 2008. Acupuncture in polycystic ovary syndrome: current experimental and clinical evidence. J. Neuroendocrinol. 20, 290–298.

Stener-Victorin, E., Jedel, E., Janson, P.O., Sverrisdottir, Y.B., 2009. Low-frequency electro-acupuncture and physical exercise decrease high muscle sympathetic nerve activity in polycystic ovary syndrome. Am.J.Physiol.Regul.Integr.Comp.Physiol. 297 (2), R387R395.

Zhao, H., Tian, Z.Z., Chen, B.Y., 2003a. An important role of corticotropin-releasing hormone in electroacupuncture normalizing the subnormal function of hypothalamus–pituitary–ovary axis in ovariectomized rats. Neurosci. Lett. 349, 25–28.

Tags:  acupuncture  fertility  Infertility 

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