heart disease

Do Statins Induce Atherosclerosis and Heart Failure?

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Statins are some of the most popularly prescribed medications on the market with 1 in 4 Americans taking statin drugs (2011). Do they work? To read the read the early reports statins were wonder drugs, capable of reducing heart attack and extending lifespan with few side effects. No need to change one’s diet or lifestyle, simply take a statin and live longer.

Over the years, the statin market has expanded to include kids as young as 8 years old: “statin therapy is considered first-line treatment for pediatric patients with abnormal lipid levels.” When combined with our love affair with vaccines, the latest proposal includes a cholesterol vaccine for children at risk for heart disease. And since 75% of Americans are still not heeding the anti-cholesterol warning, intense industry lobbying successfully changed the risk equation for statin prescriptions, immediately expanding the market potential by millions more Americans and billions of additional revenue.

Statins for Health – Maybe Not

With 1 and 4 Americans taking statins and cholesterol levels presumably controlled to within the designated healthy ranges, one might expect a concomitant reduction in heart disease and heart disease related mortality across the population. One would be wrong. Despite controlling cholesterol, Americans are as unhealthy as ever, living with increasingly more chronic diseases and dying at higher rates than ever before. Is it possible we were wrong about the relationship between cholesterol and heart function? Is it possible in our exuberance to offer simple solutions to complex disease processes we have been exacerbating the very conditions we seek to treat? Indeed, it is.

Over the last several years, a growing body of evidence suggests that statins are not only not the wonder drugs we had hoped for, but instead, may be quite dangerous, especially for women. Statins induce diabetes (a major contributor to the metabolic dysfunction implicated in coronary artery disease), increase atherogenesis (the buildup fatty plaques responsible for coronary artery disease), and damage mitochondria, an effect that is exacerbated by exercise. As a result, and in non-industry sponsored studies, statin use is associated with higher rates of all-cause mortality, cancer, heart attack, stroke, than non-statin use. Yikes.

Cholesterol Blues

Just how statins induce such negative effects is linked, in large part, to their primary purpose, cholesterol reduction. We need cholesterol. Cholesterol – fat, forms the structure of all cell membranes. We need healthy cell membranes. Fatty acids provide fuel for the production of mitochondrial energy – ATP. ATP is required for all cell functions. Cholesterol is the primary ingredient for steroid hormone synthesis. Steroid hormones regulate everything from reproduction to heart function to central nervous system activity. We need healthy steroid hormone systems. And if those aren’t reasons enough to reconsider cholesterol, the brain needs cholesterol. Reduce the cholesterol in the brain and brain activity deranges, as evidenced by the increasing recognition of statin induced psychiatric and cognitive sequelae. When we reduce cholesterol artificially, we diminish the functioning of every cell in the body by multiple mechanisms.

Cholesterol and Heart Attack

What about the link between high cholesterol and heart attacks? Isn’t it the cholesterol that causes the plaques that block our arteries and cause all sorts of problems? And, aren’t our high fat, high cholesterol diets to blame for this build up? Perhaps not, and especially for women. According to our good friend Kelly Brogan, atherosclerotic plaques and heart disease represent a ‘multi-factorial inflammatory problem with disparate drivers in different people.’ The latest research suggests that these plaques are ‘not merely the passive accumulation of lipids within artery walls‘ but rather represent oxidative stress (mitochondrial damage) with incessant immune mediated inflammatory signals driven by dietary and other factors. This makes sense when we consider that 90% of first time cardiac events can be prevented with dietary and other lifestyle changes and diet and lifestyle effect mitochondrial functioning significantly (the mitochondria drive inflammation).

The most recent research on diet and nutrition suggests diets high in empty calories, carbohydrates and sugars and low in fat are to blame for heart disease, not the high fat diets we have all been taught to avoid. It should be noted, however, that the relationship between fat and health is complex. Too much or too little impairs mitochondrial functioning.

But Wait, There’s More

A research group out of Japan has gone so far as to claim that statins are not only dangerous for the reasons stated above, but statins induce the very diseases they are promoted to protect against. In their most recent publication, Statins Stimulate Atherosclerosis and Heart Failure: Pharmacological Mechanisms, the researchers boldly argue that:

“statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and ‘heme A’, and thereby ATP generation.”

In English – statins block a whole bunch of important chemical reactions that induce coronary artery disease where there was none before. They argue, rather persuasively, that statins cause the very disease process that they are promoted to prevent. Whoa.

According to this research group, statins create the environment where fatty plagues grow and thrive. They derail our innate mechanisms to clear those plaques by damaging the mitochondria and, in so doing, damage the very foundation of cell function: mitochondrial energy (ATP) production. Without functioning mitochondria (which we have written about on many occasions), cell damage and cell death occur. With enough damage, tissue and organ damage ensue, and complex multifaceted disease processes develop. Mitochondria are the engines of health. ATP is the fuel. No fuel, no function. Statins damage the engine and block the fuel line.

What’s Worse?

Statins are frequently co-prescribed with Metformin (gluocophage) to reduce glucose in Type 2 diabetes. Metformin damages mitochondria and reduces ATP production even further (more on this in a subsequent post). Combined, these two drugs set the stage for chronic disease and increase the need for additional medications that will also damage mitochondria; a rabbit hole that is not easily climbed out of unless one is willing to look beyond the medical model. Remember, one of the largest global studies on heart health found that 90% of first time cardiac events in men can be prevented with dietary and other lifestyle changes, 94% in women. Diet and lifestyle. Sit with that for a moment. Diet and lifestyle changes are all that are needed for most people to prevent heart attack. Diet and lifestyle.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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This article was published originally on June 10, 2015.

Uterus and Ovaries: Fountain of Youth

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Numerous studies have shown a strong correlation between removal of both ovaries / bilateral oophorectomy (castration) and accelerated aging as measured by an increased risk of chronic health conditions. Hysterectomy / uterus removal with preservation of both ovaries is also associated with some of these chronic conditions. These include heart disease, stroke, metabolic syndrome, osteoporosis, hip fracture, lung cancer, colorectal cancer, dementia, Parkinsonism, impaired cognition and memory, mood disorders, sleep disorders, adverse skin and body composition changes, adverse ocular changes including glaucoma, impaired sexual function, more severe hot flushes and urogenital atrophy. Wow, that’s quite a list!

Ovaries: Health Powerhouses

This 2016 article titled “Study: Remove ovaries, age faster” sums up the findings of Mayo Clinic researchers proving yet again the harmful and unethical practice of ovary removal. The study found that ovary removal (oophorectomy) is associated with a higher incidence of 18 chronic conditions and should be discontinued in women who are not at high risk for ovarian cancer. Although this study cites the increase in chronic conditions in women who undergo oophorectomy before age 46, other studies have shown that oophorectomy even after menopause does more harm than good. Here is one that showed that to be true up to age 75.

The ovaries have both reproductive and endocrine functions as detailed in this International Menopause Society article. After menopause, the ovaries produce mostly androgens, some of which are converted into estrogen. Testosterone levels are more than 40% lower in women without ovaries compared to intact women. Women without their uterus likewise have lower levels but not as low as women without ovaries per this article. Estrogen therapy mitigates some but not all of the increased health risks of oophorectomy. But estrogen further reduces androgen levels increasing risk of osteoporosis and fracture. Nothing can replace the lifelong functions of the ovaries (and uterus).

The Uterus / Ovaries / Tubes Connection

The harms of ovary removal would also apply to ovarian failure that commonly occurs after hysterectomy and some other medical treatments. As previously cited, women who have had a hysterectomy have lower levels of testosterone. According to this 1986 publication, 39% of these women showed signs of ovarian failure. This study showed a nearly 2-fold increased risk of ovarian failure when both ovaries were preserved and nearly 3-fold when one was preserved. This likely explains the increased risk of heart disease and metabolic conditions as shown by multiple studies including this recent Mayo Clinic one. However, per this 1982 study, the uterus itself protects women from heart disease via the uterine substance prostacyclin. Loss of bone density is another harm of hysterectomy as shown by multiple studies such as this one.

Removal of even one ovary (unilateral oophorectomy) without hysterectomy is also harmful. Studies out of the Mayo Clinic showed increased risks of cognitive impairment or dementia and parkinsonism. Colorectal cancer is another increased risk according to this Chinese study and this Swedish one.

The Fallopian tubes appear to impair ovarian function to some degree as evidenced by Post Tubal Ligation / Sterilization Syndrome. This study shows an increase in Follicle Stimulating Hormone (FSH) after tube removal (salpingectomy).

Ovarian impairment after hysterectomy or salpingectomy is thought to be the mechanism of the reduced risk of ovarian cancer which is already rare.

The Uterus: Anatomy, Sex, Cancer Prevention

Hysterectomy is associated with other harms besides impaired ovarian / endocrine function. The uterus and its ligaments / pelvic support structures are essential for pelvic organ integrity as well as skeletal integrity. The effects on these structures and functions are detailed here and here. This article shows the many hysterectomized women lamenting their “broken bodies” – changes to their figures, back, hip and midsection pain, pelvic pain, bladder and bowel issues, and effects of severed nerves and blood vessels.

The uterus and associated nerves and blood vessels play a key role in sexuality and vibrancy. You can hear the desperation in women’s comments about the devastating sexual losses and feelings of emotional emptiness.

There is an increased risk of renal cell, thyroid, and colorectal cancers after hysterectomy. How ironic when cancer fear tactics are commonly used to market hysterectomy and/or oophorectomy.

Adhesions that commonly form after these surgeries can cause serious problems especially in the long term. Surgical complications – nerve injuries, bladder, bowel and ureter injuries, vaginal cuff dehiscence, a too short vagina, infections, hemorrhage – are more common than indicated by gynecologists.

Although “The Miraculous Uterus” article fails to mention the anatomical harms, it is otherwise “spot on.” It talks about the “ovarian conservation scam” and that “passion, love, ecstasy, the emotional essence that drives human achievement, forever after elude them.” This explains why “there’s no effective outrage against the barbarism of hysterectomy.”

Compelling Evidence of Harm

Clearly, there is compelling medical evidence that both hysterectomy and oophorectomy are destructive surgeries. Unfortunately, some hysterectomy forums censor negative posts giving a slanted view of the life shattering effects. Here is a sampling of women’s experiences on the Gyn Reform site.

The medical literature on the harms of these surgeries dates back over a century. Listed below are a small number of the numerous publications (minus the ovarian failure studies cited above). The Gyn Reform website has a fairly comprehensive list of resources on oophorectomy. Its Ovaries for Life sister site provides a good overview of the lifelong importance of our ovaries.

1912 – The Physiological Influence of Ovarian Secretion

1914 – Nervous and Mental Disturbances following Castration in Women

1958 – The controversial ovary

1973 – Osteoporosis after Oophorectomy for Non-malignant Disease in Premenopausal Women

“Oophorectomy before the age of 45 years was found to be associated with a significantly increased prevalence of osteoporosis within three to six years of operation.

1974 – Endocrine Function of the Postmenopausal Ovary: Concentration of Androgens and Estrogens in Ovarian and Peripheral Vein Blood

1978 – The emotional and psychosexual aspects of hysterectomy

1981 – Premenopausal hysterectomy and cardiovascular disease

1981 – Sexual response after hysterectomy-oophorectomy: Recent studies and reconsideration of psychogenesis

1981 – The role of estrogen and oophorectomy in immune synovitis

1982 – Prostacyclin from the uterus and woman’s cardiovascular advantage

1989 – The effects of simple hysterectomy on vesicourethral function

“The results show that simple hysterectomy is associated with a significant incidence of post-operative vesicourethral dysfunction and that there is an identifiable neurological abnormality incurred at operation which is pertinent to the subsequent disordered voiding.

1990 – Effects of bilateral oophorectomy on lipoprotein metabolism

1994 – The climacteric ovary as a functional gonadotropin-driven androgen-producing gland

1996 – Urinary incontinence in older women: who is at risk? Study of Osteoporotic Fractures Research Group

“Urinary incontinence is a common problem in older women, more common than most chronic medical conditions. Of the associated factors that are preventable or modifiable, obesity and hysterectomy may have the greatest impact on the prevalence of daily incontinence.

1997 – Bladder, bowel and sexual function after hysterectomy for benign conditions

1998 – Ovaries, androgens and the menopause: practical applications

1998 – Impairment of basal forebrain cholinergic neurons associated with aging and long-term loss of ovarian function

1998 – Influence of bilateral oophorectomy upon lipid metabolism

1999 – Estrogen and movement disorders

2000 – The hypothalamic-pituitary-adrenal and gonadal axes in rheumatoid arthritis

2000 – Risk of myocardial infarction after oophorectomy and hysterectomy

2000 – Hysterectomy, Oophorectomy, and Endogenous Sex Hormone Levels in Older Women: The Rancho Bernardo Study

2005 – Ovarian conservation at the time of hysterectomy for benign disease

Ovarian conservation until age 65 benefits long-term survival…. There is sustained, but decreasing, benefit until the age of 75, when excess mortality for oophorectomy is less than 1%.

2007 – Ovarian conservation at the time of hysterectomy for benign disease

Approximately 78% of women between the ages of 45 and 64 years have prophylactic oophorectomy when hysterectomy is performed for benign disease. Therefore, the decision to perform prophylactic oophorectomy should be approached with great caution for the majority of women who are at low risk of developing ovarian cancer.”

2009 – Ovarian conservation at the time of hysterectomy and long-term health outcomes in the nurses’ health study

In no analysis or age group was oophorectomy associated with increased survival.

2010 – Current indications and role of surgery in the management of sigmoid diverticulitis

A previous history of hysterectomy is a valuable clinical clue to the correct diagnosis as colovaginal and colovesical fistulas are rare in females with their uterus in place, as the uterus becomes a screen interposed between the inflamed colon and the bladder and vagina.”

2012 – Oophorectomy for whom and at what age? Primum non nocere

2016 – Study: Remove ovaries, age faster

2017 – Cardiovascular and metabolic morbidity after hysterectomy with ovarian conservation: a cohort study

A Harmful Practice That Won’t Die

Ovary removal / castration was introduced by Robert Battey in 1872 and “was practised widely for several decades….. Better insight into female physiology and ovarian function finally pushed the sinister operation of Robert Battey from the scene.” This publication refers to Battey’s operation as “barbaric.”

Despite the long-standing and compelling evidence of harm, these surgeries continue at alarming rates. Publications are misleading in that they report inpatient surgeries despite the large majority being outpatient (70% in 2014). This 2008 article reported that oophorectomies “more than doubled in frequency since the 1960’s.” According to results of a FOIA request by Ovaries for Life, there are over 700,000 oophorectomies every year despite there being only ~22,000 cases of ovarian cancer. Hysterectomy figures obtained by Ovaries for Life are also shocking at 830,000 in light of less than 70,000 cases of endometrial and cervical cancers.

Many media reports have questioned the high rate of these surgeries since gynecologic cancers are rare. The oldest one I could find was dated 1969. I found about three articles per decade in the mainstream media since then. According to the Athena Institute, half of U.S. medical schools in 1986 “had changed their suggestions and were now recommending a reconsideration of the common practice of ovariectomy.” Evidently, that never took hold.

Congress held two hearings on hysterectomy, one in 1976 and one in 1993. The 1993 transcripts state that the hysterectomy rate increased 250% in women ages 15 to 24 and 186% in ages 25 to 34 from 1965 to 1984! Despite these shocking statistics, it appears that no action was taken after either hearing.

According to this “Reassessing Hysterectomy” article, the Agency for Healthcare Research and Quality sponsored research and conferences on the overuse of hysterectomy in the 1990’s. This article is packed with information on the prevalence and harms of hysterectomy and oophorectomy as well as alternative treatment options. Yet, the high rate of hysterectomy has continued such that 45% of women will end up having one. Citing 2006 data, the oophorectomy rate was 73% of the hysterectomy rate.

How to End the Harm?

I’ve been researching this subject for over 10 years and sharing my experience and knowledge on various websites. It’s shocking how many women are misled and deceived into these surgeries. Age doesn’t seem to matter; younger and younger women are undergoing these surgeries. This appears to be the biggest surgical racket and women’s healthcare con as discussed here.

There are a number of issues that perpetuate the gross overuse of these harmful surgeries. These include:

  1. These surgeries and “forever after” care are very lucrative.
  2. The public has been led to believe that the female organs are disposable after childbearing is complete.
  3. Medical education and decades of practice have made these surgeries “a standard of care.”
  4. Informed consent is seriously lacking.
  5. Gynecology consent forms are open ended giving surgeons “carte blanche” to remove organs unnecessarily.
  6. We still live in a climate of gender disparity / male dominance.

As you can see from the list of publications above, some study authors have called out the practice of ovary removal as unethical. Numerous professional societies have issued guidelines discouraging its use in most women. But most have been silent on the overuse of hysterectomy despite its many harms.

Why has our government not stepped in to address this egregious harm? Women who have contacted their legislators have been met with indifference. Gyn Reform reported on their experiences with legislators and other authorities who can effect change. The non-profit HERS Foundation has been educating women and advocating for informed consent legislation since the 1980’s.

Why do insurance companies approve so many of these surgeries that are rarely necessary? Not only are the surgeries themselves expensive, treatments for the chronic after effects are costly. Reining in unnecessary treatments especially those that cause lifelong harm would go a long way towards making healthcare more affordable.

Why has Graduate Medical Education (GME) not changed their surgical requirements to favor organ preservation? Each resident must do at least 70 hysterectomies but there is no requirement for myomectomy (fibroid removal). Residents don’t need to do any cystectomies (cyst removals) either which is partly why so many women lose ovaries for benign ovarian cysts. Here are the GME ob/gyn requirements.

A popular mantra at Tufts in the 1970’s – “There’s no room in the tomb for the womb” – reflects this culture of the disposable uterus and gynecologists’ obsession with its removal. Insurance reimbursement rates are also to blame as they incentivize hysterectomy and oophorectomy over myomectomy and cystectomy. In many cases, medical management versus surgery is the appropriate course. The “Reassessing Hysterectomy” article cited above lists a number of treatment options for gynecologic problems. Revamping reimbursement rates to strongly favor organ preservation should eventually force GME to change their requirements. But how do we make that happen?

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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Lucas Cranach the Elder, Public domain, via Wikimedia Commons

The Hidden Heart Disease Risk Factor: High Homocysteine

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You may unknowingly have a ticking time bomb for heart disease flowing through your body. Right now. And you haven’t been told about it. Until now. Naturally produced in your body, a chemical substance called homocysteine often becomes elevated due to age, diet, and genetic disposition. If your homocysteine is high, you are at an increased risk of developing heart disease including heart attacks, coronary artery diseases, and strokes.

Staggering Mortality Rates

Heart disease is the number one cause of death worldwide. More than 17 million people—nine million of whom are women–die annually from heart disease.

In the United States heart disease ranks as the top killer of women. More than 500 American females die daily from heart disease. Furthermore, heart disease deaths in American women under the age of 55 continue to rise, according to a study published in the June 2013 issue of the journal Global Heart.

Why are so many people dying from heart disease? We have been educated to believe high blood pressure, high LDL cholesterol, and smoking are the primary causal culprits in causing heart disease. Physical inactivity, obesity, and excessive alcohol use also are attributed as risk factors for heart disease. But we hear little information about homocysteine as an independent factor for heart disease.

What is Homocysteine?

Homocysteine is an amino acid (a building block of protein) naturally produced in the body from a byproduct of another amino acid called methionine. Healthy amounts of homocysteine are vital in protein metabolism. However, homocysteine levels must be carefully balanced by adequate quantities of specific B vitamins.

Ideally, about half of homocysteine is recycled back into methionine (remethylation), and the other half is converted into a beneficial amino acid called cysteine (transsulfuration). This bifurcated process is dependent on specific B vitamins. Remethylation cannot occur without folate (vitamin B9) and vitamin B12. Transsulfuration cannot happen without vitamin B6. If these B vitamins are deficient, dangerous levels of homocysteine can accumulate in the body and damage the lining of the arteries, often causing heart disease.

Homocysteine Matters

In the late 1960s, Kilmer S. McCully, M.D., a young pathologist at Harvard University School of Medicine, reviewed a number of pathological findings of cases as far back as 1933 that involved young children with a genetic disorder who perished from atherosclerosis (hardening of the arteries). He discovered that elevated homocysteine damages arterial lining, causing arterosclerosis. Dr. McCully concluded that elevated homocysteine from a high animal-protein diet, more so than fats and cholesterol, was the primary cause of heart disease.

McCully subsequently published his ground-breaking conclusion in a 1969 issue of the American Journal of Pathology. By purporting such an unorthodox theory, he committed medical heresy.(1) Harvard denied him tenure, effectively firing him. Undeterred, he forged ahead, conducting research on homocysteine. He still practices medicine in the United States today.

Thanks to Dr. McCully’s tenacious efforts over the past four decades, a plethora of studies supporting his theory have been published. Landmark studies from the mid-1990s contributed to mainstream medicine’s eventual, yet delicate, embrace of the fact that high homocysteine is significant risk factor for heart disease. This research includes:

As part of the acclaimed Framingham Heart Study, researchers from Tufts University examined 418 men and 623 women, ages 67 to 96 years, to study their homocysteine blood plasma levels as well as their vitamin intake including folate, vitamin B12, and vitamin B6. The Tuft research team concluded that people with homocysteine levels greater than 11.4 µmol/L have a significant risk of having a heart attack. These findings were published in the February 2, 1995 edition of the New England Journal of Medicine.

The results of a study conducted by The European Concerted Action Project, a consortium of doctors and researchers from 19 medical centers in nine European countries, clinched the theory that Dr. McCully asserted almost two decades prior. By comparing 750 people under the age of 60 with blockages in their coronary arteries with 800 healthy persons also under 60 years old, the Project team determined that an elevated homocysteine score posed as great a risk as smoking or high cholesterol. Furthermore, people with the highest homocysteine levels had twice the risk of developing heart disease. Finally, the consortium discovered that those people who took folate, B12, and B6 supplements had a risk factor of about 66 percent less than those subjects who did not take the B vitamin supplements. The findings were published in the June 11, 1997 issue of the Journal of the American Medical Association.

What is a Healthy Homocysteine Level?

Homocysteine levels are easily evaluated by a simple test of blood plasma. Heath care practitioners can order a homocysteine test. But guess what? We are not routinely tested for homocysteine. In fact, I never had been tested for this important amino acid until I recently requested the test from my primary care physician. (Read on for my homocysteine score.)

To further exacerbate the issue of homocysteine evaluation, many clinical testing laboratories consider a healthy homocysteine value between 5 and up to 15 µmol/L. However, the upper limit of this range is highly misleading. A score of 6 µmol/L or less is optimal for homocysteine. Medical research has indicated that readings greater than 9 µmol/L indicate an increased risk for heart disease.

Reducing Homocysteine

The good news is that elevated homocysteine levels can be decreased by consuming adequate amounts of the B vitamins folate, B12, and B6. Although the daily dosage of these vitamins is dependent upon your homocysteine score, I offer general guidelines.

  • Foods rich in folate include wheat germ, lentils, sunflower seeds, spinach, broccoli, and romaine lettuce. If you are considering a supplement, note that “folate” is natural and “folic acid” is synthetic. Consider taking a daily 400-mcg folate capsule containing L-5-MTHF. (2)
  • The best food sources of vitamin B12 include sardines, oysters, cottage cheese, and tuna. When supplementing with B12, please ensure the B12 is methylcobalamin (methylB12). Many B12 supplements contain cyanocobalamin; yes, it contains a cyanide molecule. Consider taking 10,000 mcg daily of methylB12.
  • Fish and lean meats are excellent sources of vitamin B6 (pyridoxine). Consider taking a 25-mg B6 supplement.

You may recall that the amino acid methionine produces homocysteine. Too much methionine translates to excessive homocysteine. As animal protein is highly rich in methionine, it is wise to not overload animal protein consumption if the three major B vitamins are deficient.

Stunning Health Statistics

The scope of this article is limited to a brief discussion of elevated homocysteine as an independent risk factor for heart disease. However, I must tell you that homocysteine levels also affect the risk for developing a wide range of other serious medical conditions including cancer, diabetes, thyroid disorders, and Alzheimer’s disease. Let’s take a broad look at statistics.

Nestled in the spectacular western fjords of Norway, the University of Bergen houses one of the world’s leading homocysteine research centers. Since the 1990s, Bergen’s researchers have published dozens of papers reporting their homocysteine findings conducted during the University’s population-based Hordaland Homocysteine Study.

Having measured the homocysteine levels of 4,766 Norwegian men and women in their 60s a decade ago and then recorded those who lived and died, the researchers discovered that a 5-point decrease in homocysteine scores predicted, inter alia, a 50 percent reduced risk of death from cardiovascular disease as well as a 104 percent decreased risk of mortality from any disease or medical condition other than heart disease or cancer!

Are You Homocysteine Healthy?

It is not too early or too late to learn your homocysteine score. At the age of 60 and with a family history of heart disease, I requested a baseline homocysteine blood plasma test from my doctor. My score was an optimal 6µmol/L, a value that is most common in preteens! I attribute my homocysteine health score to feeding my body the folate, B12, and B6 it needs to maintain a balanced level of homocysteine.

Your level will not only predict your risk for heart and other serious diseases but it will help you understand how you can add energy and vitality to your life. Based on your homocysteine score, you can supplement with the necessary foods and/or dietary supplements that are readily available in retail and online outlets. And enjoy the benefits of being homocysteine healthy! I am glad than I am.

Footnote 1: Natural vitamins cannot be patented. Therefore, manufacturing and selling vitamins is far less lucrative than, for example, statins (cholesterol-lowing drugs.)

Footnote 2: The enzyme MTHFR (methylenetetrahydrofolate reductase) helps to facilitate the conversion process of remethylation.

Author’s Note: I wrote this overview to promote awareness of the potential heart disease risks associated with high homocysteine plasma levels. I briefly touched on the adverse effect of elevated homocysteine on the development of other serious medical conditions. If you are interested in learning more about homocysteine, I suggest reading: The H Factor Solution by James Braly, M.D. and Patrick Holford and/or The Homocysteine Revolution by Kilmer McCully, M.D.

Editor’s Note: Susan Rex Ryan is the author of the Mom’s Choice Award®-winning book Defend Your Life about the extensive health benefits of vitamin D. For additional information about vitamin D, check out our series of Sue’s articles, and visit her blog at smilinsuepubs.com.

This article was published previously on Hormones Matter in June 2014.

Copyright © 2014 by Susan Rex Ryan. All rights reserved.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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Estrogens Doth Make the Heart Grow Sweeter

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For years researchers have postulated the cardio–protective effects of the endogenous estrogens, namely estradiol.  Research published in 2012 in the journal Hypertension identifies a mechanism by which the estrogens regulate heart function. It appears that systemic estrogen receptors (ER alpha to be specific) and by association estradiol, the hormone that binds to the estrogen receptors, are necessary to regulate cardiac glucose metabolism. Glucose is critical for maintaining heart contractility and mass.

Using both ovariectomized (ovaries removed) and knockout mice (genes that regulate the receptors are knocked out or removed, producing animals without estrogen receptors), researchers found that cardiac glucose metabolism was significantly impaired. When a drug that increases estradiol actions was given to the ovariectomized animals, cardiac glucose function was restored.

Estrogen Receptors and the Heart Muscle

In another study researchers found that the number of estrogen receptors located on the heart nearly doubles during end-stage cardiac disease. Moreover, the patterns and locations of these estrogen receptors differ significantly between males and females. Since males die from heart failure more frequently and more rapidly than females, researchers speculate that the increase in cardiac estrogen receptors is a protective, compensatory reaction that slows down and maybe even prevents heart failure.

Estrogen Receptors, Glucose and the Healthy Heart

Under normal circumstances, healthy hearts derive most of their energy from free fatty acids with only a smaller percentage from glucose metabolism. During ischemic events or heart attacks, the metabolic balance switches and glucose metabolism increases significantly. Since estrogen receptors appear to mediate cardiac glucose metabolism, it is likely that circulating concentrations of estradiol, the hormone that binds to the estrogen receptor, also plays a role in heart health or, more specifically, in its ability to survive and recover post heart attack. The estrogen receptor-cardiac glucose connection may be the mechanism leading to the higher survival rates for women, especially women with higher circulating estradiol (pre-menopause).

Diabetes and Estradiol

Interestingly, in diabetic patients the metabolic pattern is reversed. Rather than an increase in glucose metabolism post heart attack, free fatty acid metabolism increases making it difficult for the heart to generate sufficient energy to recover. Researchers speculate that this may account for the increased rate of heart failure in individuals with diabetes. Indeed, in experimental (rodent) models of diabetes, research show that diabetics have lower estradiol levels. The research in humans is mixed.

Hormones Matter

These studies point to the importance of steroid hormones beyond their role in reproduction. The interplay between steroid hormones and cardiac function is but one example of many where the traditional view and nomenclature of reproductive, sex, or female hormones has become outdated and likely limits our understanding of health and disease.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

Photo by Tim Mossholder on Unsplash.

Sugar and our Hormones

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It’s Easter season, which outside of religious practices, means candy, candy and more candy for a lot of Americans. Peeps, Cadbury Eggs, jelly beans are just a few of the hallmarks of this spring holiday. But, along with our growing waistline, scientists and Americans are both scrutinizing our diet and a common culprit seems to repeatedly point back to the white stuff. Even CBS News, 60 Minutes is looking at the toxicity of sugar. Is candy and sugar in our diet really the cause of America’s obesity and health problems? It’s now estimated that the average American consumes up to 180 lbs of added sugar per year. Here’s another statistic that demonstrates the increase of sugar in our diets over the years:

  • In 1700, the average person consumed about 4 pounds of sugar per year.
  • In 1800, the average person consumed about 18 pounds of sugar per year.
  • In 1900, individual consumption had risen to 90 pounds of sugar per year.
  • In 2009, more than 50 percent of all Americans consume one-half pound of sugar per person
  • DAY—translating to a whopping 180 pounds of sugar per year!

“Walk away from the Peeps, Ma’am!” might be what you’re telling yourself, but this sugar epidemic is out of control thanks to the highly processed foods and soft drinks where sugar hides under a variety of names. Here are some fancier names for sugar:

Sucrose, high fructose corn syrup (HFCS), corn syrup, maltodextrin, maltose, syrup, mannitol, molasses, ethyl maltol, fruit juice, fruit juice concentrate, diatase, cane sugar, caramel, carob syrup, barley malt, beet sugar, C12H22O11,

But, that’s not all. There are as many names for sugar as Eskimos have for snow. As the public becomes more aware of the many dangers of sugar, the food industry has to try to hide it under different names.

Is it ironic or coincidental that this heavenly, legal substance that give us so much pleasure looks identical to illegal drugs such as cocaine, meth, heroine? In my opinion the only difference is that sugar is a legal drug. Am I exaggerating? No, actually I’m not. In a recent study where rats were given the choice between water, sugar and cocaine the rats choose … SUGAR! This is vital information for you and your family’s health because when you start cutting sugar out of your diet you will likely go through withdrawal symptoms as you would with any addictive substance. As an adult you can cope with the headaches, irritability and fatigue; but if you are cutting sugar out of a child’s diet they won’t understand what is happening to their body. Something to be aware of as a parent when you start cutting processed foods and sugary treats out of your children’s diet.

I’m sure some of you are reading this thinking, I’m not diabetic, this doesn’t apply to me. What if I told you that your high cholesterol and muffin top is more likely linked to the sugar than bacon? Interested now? To break it down barney-style, sugar (whether it be white rice, processed bread, soda, lemonade, plain ol’ sugar in your coffee) turns into glucose in your body. Your body releases insulin, a hormone, to cleanse the blood. What your body can’t use immediately as energy is stored in the liver and fat tissue of the body for later use. When you overload your system with sugar, your whole body has to work overtime to clean it out of your system and this means putting its everyday tasks aside to deal with this toxic overload. So, instead of processing healthy fats, proteins, good carbs, etc., your system is processing junk. Then, it has to do its normal jobs after that. No wonder you’re so tired and lethargic all the time – you’re forcing your whole body to work double shifts everytime you reach for that candy bar or soda!

SUGAR = FAT = HEART DISEASE/CANCER/DIABETES/OBESITY/LIVER DAMAGE/INFERTILITY/ACNE/AND MORE.

Can it get worst? Actually, yes. In 2007, Child and Family Resource Institute released findings that sugar disrupts the sex hormones as well.

“Glucose and fructose are metabolized in the liver. When there’s too much sugar in the diet, the liver converts it to lipid. Using a mouse model and human liver cell cultures, the scientists discovered that the increased production of lipid shut down a gene called SHBG (sex hormone binding globulin), reducing the amount of SHBG protein in the blood. SHBG protein plays a key role in controlling the amount of testosterone and estrogen that’s available throughout the body. If there’s less SHBG protein, then more testosterone and estrogen will be released throughout the body, which is associated with an increased risk of acne, infertility, polycystic ovaries, and uterine cancer in overweight women. Abnormal amounts of SHBG also disturb the delicate balance between estrogen and testosterone, which is associated with the development of cardiovascular disease, especially in women.”

So, what can you do? How do you beat the cravings? The first step is to remove table sugar and processed foods out of your house. If it’s not there, you can’t be tempted. The second step is educating yourself on the hidden ingredients that are actually sugar. (Here’s a scary tip – did you know that juice is depleted of all nutrients, flavor and color, stored for a year, and then artificially flavored and colored?!)   Thirdly, check out my post, Sweet Alternatives, for some healthy alternatives that will help you and your family beat that sweet tooth for good.

 

Photos Jdurham, jasoncangialosi Creative Common 2.0