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Are You More at Risk of Melanoma When You Have a Thyroid Problem?

Published on July 18, 2024

4.8K views

Melanoma and Hypothyroidism

My grandmother was diagnosed with a rare type of melanoma in 2016. By that time, I’d already been researching skin physiology and effects of skincare ingredients on skin for a number of years. Still, her diagnosis made me reconsider everything I thought I knew about skin health and I began digging back into the research with fresh eyes.

What I discovered was just how much skin reflects our internal state of health. And, how nothing within the body exists in isolation.

Hiding in Plain Sight

She’d jabbed a section of laminate flooring under her nail bed and it never healed properly. My grandma was an extra special sort of stubborn and over the next few years her treatments reminded me so much of the mantra from a popular movie “put some Windex® on it!”

Meanwhile, the wound festered. When she allowed them to, doctors chased infection until one finally had the right idea to biopsy it. I don’t think any of us were expecting melanoma. While her finger had a growth now, which honestly looked more like a deformity on her index finger something she might have been born with instead of a separate entity, all of it was flesh colored, just as light as the rest of her.

The biopsy results revealed something else though, a rare and extremely aggressive type of melanoma known as amelanotic melanoma.

This type of melanoma is flesh colored.

For amelanotic melanoma, the typical metrics employed by healthcare professionals suspicious of melanoma don’t apply because there’s no color to evaluate. Being flesh-colored, it’s harder to assess asymmetry, border irregularity, and even diameter. Alternative metrics include whether the spot itches or bleeds.

As my grandmother began receiving treatment for melanoma, I meandered onto a new path in my own personal health journey. Little did I know at the time how intertwined each of our paths were.

Weight Gain, Rashes, and Hashimoto’s Thyroiditis

After my gallbladder was removed, I thought my appetite would return. It didn’t. I’d been gaining weight for a little while even as my appetite was diminishing, and I just assumed it was due to my body not processing fats very well as gall sludge built up. I’d also gotten used to feeling bad after meals so suspected there was a psychological component to it too.

To support breakdown of fats, I tried lots of different digestive enzymes and one morning after taking one with ox bile salts, I experienced extreme GI distress. In addition, both of my earlobes swelled and a rash broke out on both shins. The GI distress subsided over the next few days along with the swollen earlobes. The rash on both shins? It persisted for two years. In that time, I had biopsies, I tried a variety of prescription and non-prescription products. None of which worked.

It took a diagnosis of Hashimoto’s thyroiditis and treatment for this autoimmune condition for the rash to disappear.

Pretibial Myxedema and Autoimmune Thyroiditis

The orange peel like rash on both of my shins was actually pretibial myxedema, a symptom more commonly seen in Graves’ disease even though it’s not unknown in Hashimoto’s thyroiditis.

Graves’ disease is an autoimmune thyroid condition where too much thyroid hormone is made (hyperthyroidism). I was diagnosed with Hashimoto’s thyroiditis, an autoimmune thyroid condition where too little thyroid hormone is made (hypothyroidism).

While pretibial myxedema is a more common symptom of Graves’ disease, myxedema (swelling and fluid retention of the skin caused by low levels of thyroid hormone) is a common symptom of hypothyroidism (regardless of etiology). Myxedema of any sort (pretibial or otherwise) is caused by a build-up of hyaluronic acid in the skin.

Hyaluronic acid (HA) belongs to the group of molecules known as glucosaminoglycans (GAGs). These molecules are main components of the extracellular matrix (ECM) providing structure to the body and a medium through which signaling molecules travel from one cell to another through the interstitial spaces. These molecules also help maintain sufficient hydration in the extracellular spaces because of their ability to bind water.

As GAGs (including hyaluronic acid) build-up in the extracellular matrix, more water is drawn into these spaces resulting in edema (swelling) due to fluid retention. In a healthy state, the body regulates both HA expression and also HA breakdown by controlling synthesis of both HA and hyaluronidase, the enzyme that breaks down HA.

Autoimmune thyroid states (both with Graves’ disease and Hashimoto’s thyroiditis) alter the body’s expression and break-down of hyaluronic acid. Low levels of thyroid hormone (like in Hashimoto’s and other non-autoimmune hypothyroid states) also impact hyaluronic acid expression and breakdown. In both hypothyroid states and in autoimmune thyroid conditions, HA expression and breakdown is altered in a way that allows for build-up of hyaluronic acid in tissues.

This goes beyond the skin and is one of the reasons for thyroid goiter and fibrinogenic build-up within the body in people who are struggling with poorly maintained autoimmune thyroid conditions and hypothyroidism. Build-up of HA is also associated with a variety of other autoimmune conditions including: Rheumatoid Arthritis, Type I Diabetes, Primary Sclerosing Cholangitis, and Multiple Sclerosis.

And, altered expression of hyaluronic acid, which allows reforming of the ECM, is also a way that cancer cells proliferate and spread.

Going back to look at melanoma again, hypothyroidism is linked to an increased risk of developing melanoma. The thyroid makes 3 different hormones: T3, T4, and calcitonin. Typically, T3 and T4 are given the most focus.

There are several theories on why and how sufficient levels of both T3 and T4 act to reduce the development and progression of melanoma. Both T3 and T4 regulate cell differentiation, growth, and metabolism and also modulate immune response. It’s believed that the immune modulating effects of these two hormones alters migration of melanocytes (the melanin producing cells of skin). Melanocyte migration is important to development and spread of melanoma.

This gives rise to another question… is sun exposure to blame for melanoma?

It turns out there are many different types of melanoma. The World Health Organization (WHO) now classifies melanoma into nine different categories with only three related to cumulative sun damage. If it’s possible that other factors like low thyroid also increase the risk of melanoma and reduce patient survival rates, why are we overlooking this connection?

Undiagnosed low thyroid is a common cause of many health symptoms and unfortunately, our medical establishment has been trained to test TSH (thyroid stimulating hormone), a hormone produced by the pituitary as the end-all-be-all for determining healthy thyroid function.

I myself struggled for years to find a practitioner who knew to test for anti-thyroid antibodies to rule out autoimmune thyroid condition, and it was years after discovering I in fact had Hashimoto’s thyroiditis before I found a doctor who knew how to treat the condition properly.

In her early 40s, my grandmother was diagnosed with thyroid cancer. At this point, I’m not sure anyone remembers which type of thyroid cancer she had, but certain thyroid cancers are associated with an increased risk of melanoma and for as long as I knew her, she was treated with T4 only after her thyroidectomy. In my heart of hearts, I believe my grandmother’s melanoma started because of long-standing inflammation due to that jab with the piece of laminate flooring. I also wonder… would she have been spared progression of that melanoma if her doctors factored in the thyroid piece? Would cutting edge therapy have failed if she’d been receiving T3 and T4 replacement therapy or natural desiccated thyroid? I don’t know the answer to those questions, but it seems to me that we ought to be considering these possibilities.

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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 and like it, please help support it. Contribute now.

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Glyphosate Induced Obesity?

by Chandler Marrs, PhD

Published on October 3, 2019

20.9K views

Are you struggling with your weight? Are you eating well and exercising but still not losing weight? Well then, it might be time to consider what’s on or in what you are eating or what you are eating eats. Sound complicated? It’s not. An emerging body of evidence shows a strong link between eating foods sprayed with commercial herbicides and eating meats raised on commercial feedlots (that are born and bred on a cocktail of chemicals) and obesity.

After years of eating highly processed and chemically laden fruits, vegetables and meats, the bacteria in our guts shift radically towards a species that emit what are called endotoxins. These endotoxin releasing bacteria induce inflammation, which then shifts a series biochemical pathways that favor fat storage as a protective and compensatory reaction to the steady state of chemicals coming from our diet and the lack of nutrients contained within these foods. Indeed, what we now call autoimmune reactions, the continued elevation in inflammation and antibodies, may be a result of the food we eat (and the other pharmacological and environmental chemical exposures). It turns out, that the constant state of inflammation many of us find ourselves in is the body’s way of trying to clear those toxins.

With obesity in particular, there have been several interesting studies published over the last couple years providing clear links between chemical exposures and fat storage. Whether the body stores fat or uses fat depends upon the balance of good and bad bacteria in the gut and that balance is predicated heavily upon nutrient availability and toxic exposures. High calorie, low nutrient, chemically dosed foods, shift bacterial communities that increase fat storage and inflammation. Not only that, but since gut bacteria metabolize dietary vitamins and even synthesize vitamins from scratch on their own, the high fat, low nutrient, chemically laden diet downregulates the vitamin producing bacteria, in favor of the more pathogenic and opportunistic bacteria. This further depletes nutrient stores while enhancing inflammation. The cycle becomes very difficult to end, as anyone struggling to lose weight knows all too well. There is hope, however. New research from disparate sources demonstrates how reducing the toxic load and increasing nutrient availability can re-calibrate fat usage and storage parameters.

Gut Bacteria and Obesity

Just a few years ago, researchers from Shanghai, China identified one of the gut bacterial over growths associated with obesity and published their results in a paper entitled: An opportunistic pathogen isolated from the gut of an obese human causes obesity in germfree mice. Called enterobacter clocae, the endotoxin producing bacteria was found overpopulated in the gut of a severely obese patient who was also insulin resistant, hypertensive and suffered from the array of obesity related health issues. The enterobacter clocae pathogens made up 35% of the total bacterial content in this patient’s gut; a huge bacterial load. Knowing that enterobacter emitted endotoxins and that endotoxins were associated with inflammation and insulin dysregulation, the researchers speculated that a reduction in the enterobacter population would correspond with a reduction in weight and the other health issues. They were correct. With a special diet and traditional Chinese herbs, weight loss and health parameters changed along with the reduction in toxic load. After 9 weeks, enterobacter represented only 1.7% of the total gut bacteria and at 23 weeks, .32%. The total weight loss during that period was 50kg or 110lbs.

Could something as simple as reducing the opportunistic enterobacter via diet be the solution to obesity? To answer this question, the researchers went back to lab and designed an experiment to test the hypothesis, only they did it in the reverse. They asked if enterobacter was a causative factor in obesity, could they induce obesity in mice bred specifically to resist excessive weight gain simply by increasing the bacterial load?

From the fecal matter of the obese patient, the researchers isolated the particular strain of enterobacter clocae called B29. They took the B29 and inoculated four groups of seven, germ-free mice; B29 inoculated plus normal diet or high fat diet and non-inoculated normal or high fat diet. Germ-free mice are a strain of mice that are microorganisms free and raised in isolates. They are resistant to obesity even when fed a high fat diet.

One mouse from each of the inoculated groups died immediately after the inoculation indicating the toxic nature of this bacteria. Remember, this strain of bacteria represented 35% of the original patient’s gut bacteria, likely acquired gradually over the course of lifetime. During the first week, all of the inoculated mice lost weight, again indicating the mounting immune response. Anorexia, is often a sign of illness as the body reallocates resources towards fighting an infection.

Subsequently, and after the immediate anorexic responses, both groups of inoculated mice gained excessive weight, whereas the non-inoculated mice did not. The inoculated plus high fat diet group not only gained significantly more weight but expressed higher levels of enterobacter inflammatory markers and insulin resistance showing an interaction between diet and bacterial growth. The researchers speculate that the high fat diet facilitates the transfer of this bacteria to the bloodstream and increases the systemic inflammatory reaction. The inflammation then shifts the body towards fat storage via a range biochemical cascades meant to fight the infection but that also induces other reactions along the way; reactions we consider hallmarks of metabolic disease including high cholesterol, insulin resistance, liver damage, decreased adiponectin (satiety hormone – low adiponection means one is always hungry) and even increased amyloid A proteins associated with Alzheimer’s. This study, albeit small and in need of replication, shows us that when the balance of good to bad bacteria shifts, obesity is induced. It doesn’t tell us, however, how environmental chemicals in and on food impact this bacterial shift. For that we have to go to a couple other reports.

Nutritional Perils of the Western Diet

The Western diet has become a synonymous with highly processed foods that barely resemble actual food in nutrient and DNA composition. Indeed, in our efforts to produce the largest and prettiest produce, we’ve cultivated out 95% of the genetic variation from food crops; reducing to almost nothing the ~200,000 plant metabolites that provide nutrition. To make matters worse, we have substituted nutritionally rich and diverse crops with ones that originate from plant seeds engineered with bacterial RNA and DNA and are laced with glyphosate, adjuvants and other chemicals. In addition, all commercial meat production relies heavily on genetically modified, glyphosate-doused feed to grow the cattle, combined with prophylactic antibiotics, growth hormones and a cocktail of other chemicals that compensate for the deplorable conditions under which Western foods are produced. The genetically modified, chemically laden food stuffs are then sold to the consumer as fruits, vegetables, meats and dairy or processed even further into other food-like products. From beginning to end of the food chain are exposures to chemicals and foreign bacterial DNA that our bodies cannot accommodate and that provide only limited nutrients.

So, in addition to the direct exposure to chemical toxicants, conventionally grown Western foodstuffs also impair health by reducing vital nutrient content required for even the most basic cell functioning. By disrupting the balance between good gut bacteria and bad or pathogenic bacteria conventionally grown further disrupts nutrient availability while increasing inflammation and the cascade of ill-health is set in motion.

Metabolic Starvation in the Face of Obesity

As we’ve covered previously, every cell in the body requires energy to exist and function. That energy comes in the form of mitochondrial adenosine triphosphate or (ATP). The production of ATP requires nutrients as co-factors and for enzyme functioning. Many of these nutrients come from diet and others are produced de novo or from scratch by the bacteria in our gut. Glyphosate grown foods attack both. Glyphosate reduces the nutrient availability of foodstuffs, even in the less processed, presumed healthy fruits and vegetables, while simultaneously killing the good bacteria in our guts. Glyphosate is a potent bactericide that in a perverse twist of design preferentially targets the beneficial bacteria while leaving untouched the opportunistic and pathogenic bacteria, like enterobacter clocae. So while eating a healthy diet might lead to weight loss and improved health outcomes under normal circumstances, when that diet consists of conventionally grown foods, with genetically engineered seeds capable of withstanding the toxic insults of glyphosate and its adjuvants, neither the diet nor the disrupted intestinal flora can produce the nutrients required to enable healthy cellular metabolism. The GM-glyphosate combo induces a state of metabolic starvation and through a number of survival pathways and shifts towards fat storage rather than fat loss as a secondary source of energy.

Critical to this entire equation is the fact that the bactericidal properties of glyphosate disrupt normal gut microflora. Glyphosate directly shifts the balance of power away from the healthy, vitamin and mineral factories that feed the body’s enzymes and mitochondria, towards more pathogenic bacteria that are resistant to glyphosate and may even feed on it, further evoking metabolic starvation. As the bacterial balance continues to shift, disease appears and inflammation ensues. Those diseases are then treated pharmacologically with drugs that also disrupt gut bacteria, deplete nutrient stores and damage mitochondria. The cascade of ill-health becomes more and more difficult to end using traditional approaches. Moreover, where and how disease appears is as much based upon individual predispositions as it is on nutrition and other exposures, making the complexity of modern illness something modern medicine is not accustomed too. In other words, these diseases do not fit neatly into the one disease, one medication model, and thus, very rarely respond favorably to treatment.

To Lose Weight, Feed the Body What it Needs: Nutrients.

Despite the complexity of the interactions that come together and create the chronic health issues we face today, there is one variable that can be controlled that will mitigate obesity and ill-health directly: eating, or more specifically, what is eaten. The simple act of cleaning up one’s diet, of moving away from processed foods and away from conventionally grown foods towards organics, can have a tremendous effect on reducing the body’s toxic load and subsequent inflammation, weight gain, and disease. Similarly, replacing needed micronutrients so that bacterial and mitochondrial functioning can come back online and switch from fat storage to fat/energy burning will be critical. This will take time, however, and the transition towards health may be slow. Obesity and ill-health did not emerge overnight and they will not disappear overnight. Finally, we have to recognize that there is no one-size-fits-all, silver bullet, diet vitamin or diet pill. Each of us adapts to chemical exposures and the lack of nutrition individually and uniquely. So each of us requires a different cocktail of nutrients to move forward. Which nutrients and at what doses should be determined individually and may involve some degree of trial and error. As the Western diet is devoid of critical vitamins, minerals and amino acids, it is likely many individuals are suffering from broad based deficiencies. It is also likely, that restoring what has been absent chronically will go a long way towards health and healing, regardless of one’s particular health issues. So if you are struggling with obesity and other health issues, feed your body what it needs to function – nutrients.

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 i yunmai on Unsplash.

This post was published originally on Hormones Matter on July 28, 2014.

Weight Gain and Hormonal Contraceptives

by Kerry Gretchen

Published on June 8, 2016

7.7K views

Once upon a time, a 26-year-old woman went to her doctor and asked to be put on the new birth control pill that allowed women to only have four periods a year. She had seen it advertised on television. Four months later, 15 pounds heavier and suffering from mild depression, she returned to the doctor feeling miserable. The doctor told her the weight gain and depression were not from the pill because those were not side effects of hormonal birth control. This left the young woman feeling like it was her fault she had gained weight. Needless to say, that didn’t help with the depression. But she switched back to her original birth control pill and lived happily (but heavily) ever after. Well, until it gave her a stroke two years later.

I’ve written a lot about my stroke and about blood clots and birth control pills, but there are many other side effects from hormonal birth control. More often than not, we are told that these side effects do not exist; that they are all in our heads. Are they? Or are we simply being ignored and lied to?

What Does The Research Show?

When researching my thesis, I was interested in finding out what women knew about the risks associated with birth control pills. I created a survey based on a published study by researchers in this field. The original study outlined which side effects were and were not associated with birth control pills. The survey used in my thesis demonstrated the following:

“When the women were asked to select which risk factors were associated with birth control pills, most women, 76.7% of the 313 who answered the question, selected blood clots. Weight gain, which is not considered a health risk or even a side effect of birth control pills, was the selection most chosen (79.9%).”

The number one answer most women chose was weight gain, yet all the research I read said that weight gain was not a side effect of birth control pills. My own doctor had told me it wasn’t a side effect when I stood before her 15 pounds heavier after switching pills. Even as I wrote my thesis, I wondered how we could all be so wrong. Well, it turns out we weren’t. The pill can cause weight gain. And they knew it could, even back in 1970. The following is testimony from the Nelson Pill Hearings.

Dr. Francis Kane (page 6453): [In a Swedish study of 344 women] Of the 138 women who stopped using the medication, weight gain and emotional disturbances were the most frequently reported, 26.1 percent and 23.9 percent.

Dr. Louis Hellman (page 6203): My private patients… come off the pill because of a host of minor reactions. The most prevalent one is weight gain. The modern American girl just does not want to gain 5 or 10 pounds if she can help it.

What About Today’s Birth Control Pills?

I took another look at what I could find out about weight gain and hormonal contraception now. According to WebMD:

“When birth control pills were first sold in the early 1960s, they had very high levels of estrogen and progestin. Estrogen in high doses can cause weight gain due to increased appetite and fluid retention. So, 50 years ago they may indeed have caused weight gain in some women. Current birth control pills have much lower amounts of hormones. So weight gain is not likely to be a problem.”

Maybe larger doses of hormones cause more weight gain. But I don’t think that means that smaller doses cause none. And what about taking that smaller dose for a decade or more?

Most current medical information dismisses weight gain completely. On the Mayo Clinic website’s FAQ page for birth control pills it says:

“Do birth control pills cause weight gain? Many women think so. But studies have shown that the effect of the birth control pill on weight is small — if it exists at all.”

That’s right, ladies. Just like your menstrual cramps, weight gain on the pill probably doesn’t exist. But wait, the Mayo Clinic says there are studies that show hormonal contraceptives don’t cause weight gain. Where are these studies?

Inconclusive? Or Incorrect?

A recent meta-analysis (2014) conducted by Cochrane (an independent group that reviews randomized controlled trials and organizes medical research information) found the following:

Available evidence was insufficient to determine the effect of combination contraceptives on weight, but no large effect was evident. Trials to evaluate the link between combination contraceptives and weight change require a placebo or non-hormonal group to control for other factors, including changes in weight over time.

You mean to tell me in the 40+ years since the Nelson Pill Hearings we haven’t been able to conduct one conclusive study to determine how hormonal contraception affects weight? Perhaps it’s time to start asking why. All those studies that provided insufficient evidence, who funded them and who might stand to lose if they were conclusive? I don’t know for sure but I do know that one of the few things women fear as much as an unintended pregnancy is weight gain. Even the staunchest feminists among us often fret over our figures.

According to Naomi Wolfe’s The Beauty Myth, “thirty-three thousand American women told researchers that they would rather lose ten to fifteen pounds than achieve any other goal.” Setting aside how disturbing that is, we can easily see how the fact that hormonal birth control can cause weight gain might adversely affect the pharmaceutical industry’s bottom line (pardon the pun).

At the Nelson Pill Hearings, there were at least a half dozen experts–doctors specifically chosen to testify before Congress–that mentioned weight gain as a side effect of the birth control pill. Including ones who admittedly worked for the pharmaceutical industry. But now, nearly five decades later, the research is inconclusive. Doctors are telling patients that hormonal contraceptives are not responsible for weight gain, yet 80% of women surveyed thought that weight gain was a side effect. Like so much surrounding the pharmaceutical industry, something doesn’t add up here. And who is paying the difference? Women. Yet again we are being told that it’s all in our heads. Have you had experience gaining weight on hormonal birth control?

Further Testimony on Weight Gain

This testimony from the Nelson Pill Hearings just scratches the surface of the side effects caused by hormonal contraceptives. I’ll be expanding more on a lot of this testimony in future articles. But perhaps Dr. Victor Wynn explained most succinctly how these side effects manifest when he testified (page 6303):

When I say these changes occur, I mean they occur in everybody, more in some than in others, but no person entirely escapes from the metabolic influence of these compounds. It is merely that some manifest the changes more obviously than others.

Dr. Robert Kistner (page 6082): I tell her about the side effects plus a weight gain edema and I may even give her a prescription for this.

Dr. John Laragh (page 6165): We do not have any firm clues. But it does look as though those who accumulate salt and water and gain weight on the oral contraceptives might be especially vulnerable [to increased hypertension].

Dr. Francis Kane (page 6449): Complaints of moodiness, being cross and tired, alterations in sexual drive, weight gain, edema, and insomnia were commonest in the group using the estrogen-progestin group.

At the hearings, Dr. Herbert Ratner (page 6737) was asked by James Duffy, minority council:

Mr. Duffy: You use the word “disease” here. Disease to me seems to be a pretty strong word and I am just curious why you would consider weight change to be a disease?

Dr. Ratner: You realize that obesity is one of our major problems in this country.

Real Risk Study: Birth Control and Blood Clots

Lucine Health Sciences and Hormones Matter are conducting research to investigate the relationship between hormonal birth control and blood clots. If you or a loved one have suffered from a blood clot while using hormonal birth control, please consider participating. We are also looking for participants who have been using hormonal birth control for at least one year and have NOT had a blood clot, as well as women who have NEVER used hormonal birth control. For more information or to participate, click here.

Menopause and the Body Fat Blues

by Chandler Marrs, PhD

Published on June 26, 2013

9.8K views

Postmenopausal weight gain is a common problem for many women. Most suspect it has something to do with declining or changing hormones, but the mechanisms have remained unclear. Fat, researchers are learning, is not merely the inert blob we thought it was, but a complex endocrine organ capable of initiating and maintaining its own growth. Not good news for those of us who carry an over abundance of this cushy substance.

In a recent study measuring the mechanisms of subcutaneous thigh fat storage it was learned that the enzymes that direct whether we store or burn fat are re-regulated post menopause, presumably by hormone changes. Called adipocyte fatty acid storage factors, these proteins determine whether and how much fat is burned or stored. For post menopausal women, not only are there more post meal fatty acids but more fat is stored. What was interesting was the mechanism. There were no differences between the pre- and post- menopausal enzymes that broke down the fats (lipoprotein lipase), meaning the capacity to burn it remained unchanged. What changed was the capacity to store it.

The researchers found the two enzymes that determine fat storage rates (adipocyte acyl-CoA synthase and dicylglycerol acyltransferase) were significantly upregulated in postmenopausal women. Why they were upregulated was not clear. The standard presumption was made that declining ‘estrogen’ concentrations must somehow regulate the fat storage enzymes, but none of the estrogens were measured.

In a similar study looking at the role androgens and fat storage in men (diagnosed hypogonadal – low testosterone and eugonadal – ‘normal’ testosterone men), researchers found the hypogonadal men exhibited upregulated fat storage factors in the femoral area (butt and thigh). The pattern was consistent to that observed in postmenopausal women. Since neither testosterone, the other androgens or estradiol and other estrogens or even progesterone hormones were measured in either study, it is unclear which hormones or hormone patterns impact these fatty acid storage factors. What is clear, however, is that aging, whether chronological or endocrine, seems to increase fat storage.