SpectraCell Blog

PCOS: Addressing the Root Cause

Posted by SpectraCell Laboratories, Inc. on Mon, May 13, 2019 @ 02:08 PM

AdobeStock_98525490What exactly is PCOS?

One of the most common endocrine disorders in young women and leading cause of infertility in American women of childbearing age is the condition known as PCOS (polycystic ovary syndrome). Like other syndromes, PCOS is actually a cluster of symptoms, most notable of which is an unusually high level of androgen hormones (male sex hormones) in women. The name originates from the presence of ovarian “cysts”, which are actually immature egg follicles that never descend into the uterus, remaining in the ovary and thus appearing as cysts. Ovulation does not occur in women with PCOS, so these follicles that normally turn into a corpus luteum (egg ready for fertilization) remain undeveloped and consequently, infertility results.

What role do androgens play in this unique syndrome?

The key diagnostic criteria for PCOS is high androgen levels, although the role of androgens in women is commonly misunderstood. The most potent androgen hormone is testosterone, and thus androgen hormones are typically thought of as male hormones, although androgens (including but not limited to, testosterone) exist and serve an important role in women as well. But in PCOS patients, the androgen levels have become too high relative to other hormones. DHEA and androstenedione (important precursor hormones to estrogen) are also androgens, existing in both male and females.

How does PCOS present clinically?

Clinical manifestations of PCOS include acne, oily skin, unusual facial hair in women from the high testosterone (also known as hirsutism), infertility, insulin resistance and obesity. From a hormone perspective, women with PCOS will have high testosterone levels. In addition, they tend to be obese. Since fat cells contain the hormone aromatase which converts testosterone to estrogen (this occurs in adipose tissue of both men and women and is called aromatization), PCOS women can have high testosterone and high estrogen. Another hallmark of PCOS is insulin resistance (precursor to diabetes) which contributes markedly to weight gain and obesity. Since insulin resistance is indicative to poor glycemic control, reversing the blood sugar regulation dysfunction that occurs in PCOS is paramount to treatment.

Other hormone indications in PCOS patients is high luteinizing hormone (LH) and low follicle stimulating hormone (FSH). Hyperandrogenic women (high testosterone) with PCOS tend to have low serum SHBG concentrations as well.

What role do micronutrients play in treating PCOS?

PCOS is first and foremost a hormone-linked syndrome. Micronutrients profoundly affect hormones, including insulin – the hormone responsible for shuttling blood glucose into cells. When insulin is chronically high, it becomes the key contributor to weight gain and metabolic dysregulation that is associated with PCOS.

Inositol is a B-complex associated nutrient that plays a very important role in cell to cell communications, which work hand-in-hand with hormone signaling. Studies indicate that exogenously administered inositol improves insulin activity (dosages of 1200 mg D-chiro-inositol were assessed).1 Evidence even goes to far as to suggest that insulin resistance in PCOS is due to inositol deficiency and that repletion of this key nutrient can significantly improve circulating hormone levels and ovulation rate.

Lipoic acid is another key nutrient in the treatment of PCOS. It enhances glucose uptake into muscles, improves insulin sensitivity and lowers triglycerides. Similarly, vitamin D deficiency is common in PCOS. This vitamin, which is actually considered a pro-hormone helps normalize the menstrual cycle. Chromium has been shown to benefit clinical manifestations of PCOS as well by facilitating the binding of insulin to receptors in the body, thus improving insulin sensitivity.

In reality, any nutrient that affects hormone production, weight management, fertility or glycemic control will potentially impact PCOS as well.

How to address the problem

Having a complete hormone panel run, along with a micronutrient analysis would be a good starting point in understanding what imbalances need to be addressed and how to correct them. Order your tests today! 

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Interested in learning more about PCOS? Register for our upcoming webinar on The PCOS Environmental Roadmap: How to Reverse PCOS and Begin Recovery.

References

1. Nestler JE, Jakubowicz DJ, Reamer P, et al. Ovulatory and metabolic effects of D-chiroinositol in the polycystic ovary syndrome. N Engl J       Med 1999;340:1314-1320.

2. Masharani U, Gjerde C, Evans J et al. Effects of controlled-release alpha lipoic acid in lean, nondiabetic patients with polycystic ovary syndrome. J       Diabetes Sci Technol 2010;4:359-364.

3. Fang F, Ni K, Cai Y et al. Effect of vitamin D supplementation on polycystic ovary syndrome: A systematic review and meta-analysis of randomized      controlled trials. Complement Ther Clin Pract 2017;26:53-60. 

4.  Lydic M, McNurlan M, Bembo S et al. Chromium pioclinate improves insulin sensitivity in obese subjects with polycystic ovary syndrome. Fertil     Steril 2006;86:243-246.

Topics: Nutrition, endocrine disorder, Functional Medicine, Hormone Imbalance, Intracellular Micronutrient Testing, Polycystic Ovary Syndrome, PCOS, PCOS and Micronutrients, PCOS and Insulin Resistance

Cellular Levels of Vitamin B1 May Influence the Progression of Huntington's Disease

Posted by SpectraCell Laboratories, Inc. on Thu, May 17, 2018 @ 01:38 PM

Vitamin_B1Huntington’s disease is a relatively rare disease that occurs when a person has altered expression of a specific gene called the huntingtin gene. The presence of this mutated gene initiates the synthesis of an altered protein  (similarly called the mutated huntingtin protein, or mHTT) that damages nerve cells in the brain over time. The disease progresses over the course of several years and clinically manifests as gradually worsening mental, emotional and physical dysfunction, to the point of total incapacity.

In this experiment, scientists studied the effect of supplemental vitamin B1 (thiamine) on B lymphocytes (white blood cells) that carried the mutated Huntington gene and compared them to normal B lymphocytes that did not carry the mutated gene, which served as the control. The scientists supplemented vitamin B1 on the two sets of cells and compared the following: (1) cell growth rates, (2) vitamin B1 intake into the cell, (3) genetic profile of 27 different thiamine related genes and (4) the enzyme activity of several B1-dependent proteins.

They found that supplemental vitamin B1 stimulated more of an increase in growth in the mutated Huntington gene cells than the control cells, suggesting the Huntington cells had a higher requirement for vitamin B1. In addition, vitamin B1 intake, and therefore intracellular levels, was increased in the Huntington cells compared to control. Enzyme activity did not differ between cell types, but the expression of genes related to B1-dependent energy metabolism did differ between the control and mutated cell groups.

Vitamin B1 is known for its role in energy metabolism and deficiency has been linked to a several neurological syndromes such as Alzheimer’s disease and Wernicke encephalopathy, which suggests it may play a role in Huntington’s disease. Although this study was done in vitro (in test tubes), the increased expression of B1-related genes upon supplementation of B1 suggests intracellular vitamin B1 levels may play an important role in the manifestation of this enigmatic disease.

(Advances in Clinical and Experimental Medicine, August 2017) 
 Role of thiamine in Huntington's disease pathogenesis: In vitro studies.

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Topics: micronutrient testing, Vitamin B1, Vitamin B1 Deficiency, Functional Medicine, huntington's disease, vitamin b1 and huntington's disease, energy and metabolism, micrnonutrients

Your Medication’s Side Effects Might Be a Drug-Induced Nutrient Deficiency

Posted by SpectraCell Laboratories, Inc. on Tue, Apr 24, 2018 @ 03:34 PM

rx drugs

Pharmaceutical medications help millions of Americans cope with clinical symptoms every day, but most are not without side effects.  In fact, the side effects of a medication are often worse than the original condition according to many patients.  One reason for this is that prescription drugs very often cause nutrient depletions, which manifest clinically in very significant ways.  A classic example is coenzyme Q10 deficiency caused by statin medications.  Statins block an enzyme that affects cholesterol production, but the same enzyme is needed to manufacture the important antioxidant coenzyme Q10, which is a key nutrient needed for cellular energy metabolism proper heart function.   So if you block this enzyme (called HMG-CoA reductase for hydroxyl-3-methylglutaryl coenzyme A, which is why statins are known generically as HMG-CoA reductase inhbitors), you may lower cholesterol, but as a consequence you may cause a coenzyme Q10 deficiency, which can manifest as low energy and muscle pain. 

Why is this so common?  The reason is simple – the pharmaceutical approach is fundamentally different from the nutrient repletion approach in that medications alter or interrupt metabolic pathways to achieve a clinical result while nutrient repletion supports or helps maintain the optimal function of a metabolic pathway to achieve balance.  In general, medications are palliative in that they focus often on the relief of symptoms.  Conversely, nutrient repletion is curative and the goal is optimal cellular function of which a side effect is relief of symptoms. 

This is not to say that medications have no place in health, but they do have a role in nutrient depletion which can cause the unpleasant and dangerous side effects.  Especially in the age of polypharmacy – when people take more than one medication simultaneously (including over the counter meds) – nutrient depletions caused by drugs deserve a closer look.  Here are some examples of how medications can deplete micronutrients:

  • Meds can interrupt endogenous production of a nutrient (statins and CoQ10)
  • Meds impairs absorption in the gastrointestinal tract (antacids and B12)
  • Meds can create reactive oxygen species and thus “use up” antioxidants (NSAID and cysteine)
  • Meds can increase urinary excretion of nutrients (diuretics and minerals)
  • Meds can alter the gut microbiome (antibiotics and vitamin K)
  • Meds can impairs mitochondrial function and cellular respiration

Adding to the problem is that fact research on drug-induced nutrient depletions is comparatively sparse compared to the giant funding allotted to pharmaceutical development and testing. In addition, there is a lag time between the market introduction of a blockbuster drug and potential nutrient depletion-induced side effect data.  An example of this is research in the past decade that implicates antacids (proton-pump inhibitors) as a causative factor in cardiac events due to their tendency to deplete magnesium.  The strong link between PPI use and arrhythmias (irregular heartbeat) may be caused by magnesium depletion, which may also explain an increased risk in bone fractures for people on long-term PPI use according to the FDA.  Although research on PPI-induced magnesium deficiency emerged in the last few years,  PPIs have been widely used in the market since 1990.  In some cases, the research on drug-induced nutrient depletions may not emerge for many years after a drug is widely accepted into the market.

If you are taking a medication, have your micronutrient levels tested today.

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For more information on drug-induced nutrient depletions associated with statins and antacids, download our nutrient wheels! 

Statins Nutrient Wheel
Antacids Nutrient Wheel

Topics: statin, Intracellular Analysis, micronutrient deficiencies, Advanced Nutritional Testing, Effects of Statins on CoQ10, Drug-induced Nutrient Depletion, Functional Micronutrient Testing, Antacids, Functional Medicine