A thin-looking person may, despite appearing thin, have a problem in common with an obese individual: an increase in visceral fat. This type of fat has a more dangerous behavior than typical fat located under the skin: it produces hormones, inflammatory markers, and is a predictor of mortality.

The goal, therefore, is to limit an increase in visceral fat. It accumulates differently in men and women. In this article, we will however also discover what attitudes (such as resting after lunch or concentrating the daily intake of fat in one meal) can contribute to an increase of this type of fat.

Dr. Celia Gonzalo Gleyzes – Neolife Medical Team

Types of body fat

Adipose (fatty) tissue is classified as brown, beige, or white. Brown and beige adipose tissue, which are rich in mitochondria, are capable of producing heat (thermogenesis). White adipose tissue abounds in our body and as we age, brown adipose tissue is lost.

White adipose tissue, in turn, is divided into subcutaneous, visceral (intraperitoneal and retroperitoneal), and ectopic. Thus, ectopic adipose tissue is located within the organs and visceral adipose tissue surrounds them.

Subcutaneous fat is much more abundant in women.

When visceral fat accumulates, the contour of the abdomen increases, but it must also be remembered that a prominent abdomen also reflects an increase in subcutaneous fat.

The fat surrounding the heart (epicardial fat) is also considered visceral fat.

Men like apples and women like pears

Men tend to acquire a rounded silhouette because of the accumulation of fat in the trunk and in the abdomen (android obesity). Premenopausal women (of a childbearing age), on the other hand, will accumulate subcutaneous fat in the hips and in the buttocks (gynoid obesity).

However, women may also have an android phenotype, the most unfavorable at the cardiovascular level.

Visceral fat is associated with metabolic problems

Although subcutaneous abdominal fat and intrahepatic fat are associated with an increased risk of mortality in men, only visceral fat is a powerful independent predictor of mortality in this group.

Obesity can disrupt the functioning of microvascularization. Studies in animals have shown insulin resistance to decrease the density of blood capillaries and increase their permeability to macromolecules. That dysfunction can lead to the development of hypertension, one of the criteria of metabolic syndrome.

As visceral fat accumulates, macrophage infiltration (immune system cells that participate in inflammation) increases. Macrophages release inflammatory cytokines (such as TNF alfa), causing visceral adipocytes to become insulin resistant and release fatty acids. Foods rich in triglycerides would act in the same way, increasing the flow of fatty acids into the portal venous system (venous blood flow from the gastrointestinal organs and spleen to the liver before returning to the heart).

Increased fat uptake in male visceral adipose tissue

Fat accumulation is the result of low or inadequate energy expenditure leading to energy accumulation.

Fat catabolism of adipocytes, lipolysis, is mediated by epinephrine. Estrogens reduce lipolysis in the adipocytes of the subcutaneous fat of the buttocks but could increase it in adipocytes of visceral fat.

Men accumulate more fat in the abdominal visceral reserve because this area absorbs more fat in men than in women.

The activity of lipoprotein lipase (LPL) is important in fat accumulation because most of the fatty acids absorbed by the deposits comes from the hydrolysis of lipoprotein triglycerides. One study has shown that testosterone is able to suppress LPL activity and fat accumulation in the femoral region.

Women can secrete VLDL particles with triglycerides to combat liver fat overloads and they will redirect them from the liver to subcutaneous adipose tissue.

Fat is picked up by the adipocytes from the lipoproteins, lipid particles with triglycerides inside. The organ that secretes the most fat, especially postprandially (after eating), is the small intestine. In women, 5% of ingested fat is stored in intraperitoneal visceral fat but in men that figure comes to 21%.

Absorbed fat is secreted by the enterocytes in two forms: chylomicrons (larger in size) and VLDLs. VLDLs can be produced between meals but chylomicrons depend on fat intake (and if the intake is high in fat, the chylomicrons will be larger in size). Thus, men consume more fat than women and their chylomicrons are larger, making displacement in the lymphatic system slower.

The lymphatic circulation system is a low-pressure system that depends on the contraction of the surrounding muscles like the diaphragm and other abdominal muscles. Prolonged elevation of plasma chylomicrons in men, as well as an increased recovery of lipids infused in the intestinal mucosa when the intestine is overloaded with fat, both support the notion that larger chylomicrons that are preserved for more time in the intestinal mucosa promote the accumulation of abdominal visceral fat.

Intestinal lymphatics with pores (typical of aging processes) allow more chylomicrons to leave the lymphatic lumen and be preserved in the extracellular matrix. Their enormous size can further prolong their retention, allowing their dietary fat to be hydrolyzed and stored by the surrounding abdominal visceral adipocytes.

Solutions to combat visceral fat

Physical exercise will act in different ways:

• Calorie consumption and activation of fat catabolism.
• Inhibition of fatty acid uptake by visceral adipose tissue.
• Reduced retention of chylomicrons in the intestinal mucosa.
• Acceleration of chylomicron transport through muscle contraction.
• Reduction of the porosity of lymphatic vessels.

As for diet, it is recommended to moderate daily fat intake in addition to splitting up fat consumption into several intakes throughout the day.

Now it is easy to understand why sumo wrestlers eat once a day and take a nap afterwards. To keep ourselves healthy and increase our life expectancy, it is better not to follow their example.

BIBLIOGRAPHY

(1)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906176/#:~:text=In%20other%20words%2C%

20women%20accumulate,up%20more%20fat%20than%20women. Nauli AM, Matin S. Why Do Men Accumulate Abdominal Visceral Fat? Front Physiol. 2019;10:1486. Published 2019 Dec 5. doi:10.3389/fphys.2019.01486

La entrada Visceral Fat: The Enemy se publicó primero en Neolife.

The prostate, the organ that gives men so much grief. Evidence shows that sooner or later, it’ll grow. Can we prevent this without the use of drugs?

It is worth explaining the elements that will induce growth in this gland called the prostate. The best medicine is preventive medicine. Monitoring infections, living a healthy lifestyle, and replenishing those hormones we lose during aging is the right course of action.

Dr. Celia Gonzalo Gleyzes – Neolife Medical Team

Anatomy of the prostate

The prostate is a glandular organ of the male reproductive system. It is chestnut-shaped, located in front of the rectum, behind and underneath the bladder.  This organ functions as a secondary bladder that puts pressure so semen may be expelled from the urethra. Moreover, it may close the passage to the bladder to prevent it from releasing its contents during intercourse.

The prostate is connected to the testicles through the vas deferens, which rise above the bladder. It surrounds the first section of the urethra, a tube through which urine and semen circulate to the penis.

It consists of different zones:

• The fibromuscular stroma extends post laterally and forms the capsule.
• The transitional zone, close to the prostate utricle and the periurethral glandular tissue.
• The central zone surrounds the transitional zone.
• The peripheral zone occupies 75% of the total volume.

Androgens: their role in prostate development and growth

The effect of androgens in mesenchymal cells is necessary for the formation of the prostate, but also for its growth. Three growth episodes are distinguished: the first occurs in the fetal stage, the second during puberty, and the third begins in middle age and is sustained during aging. The first two episodes are associated with increased testosterone.

The male fetus begins to produce testosterone in the eighth week of gestation, reaches a peak in the 16^th week (adult-like concentration) and then decreases to low levels at birth. A short time after birth, testosterone increases again for six months and then drops to undetectable levels during childhood.

The androgenic environment is responsible for the differentiation of the male reproductive system (internal and external), including the prostate. Differentiation and prostate growth begin at week 10-12 of gestation and are considered complete at birth.

What is truly striking, with respect to other organs, is that the prostate continues to grow in adulthood. In the third phase of growth, the transitional zone increases in size, and this time, there is no testosterone spike but quite the opposite: the levels drop.

Lower testosterone and prostatic hyperplasia during aging

Intraprostatic androgen levels in patients with benign prostatic hyperplasia are no different than those in unaffected patients.

Testosterone is converted into estradiol through the enzyme called aromatase.

Two estrogenic receptors (ER-alpha and ER-beta) are expressed in the prostate. ER-alpha is detected in stromal cells, and when stimulated, it is associated with hyperplasia and inflammation. By contrast, inactivation of the ER-beta receptor leads to hyperplasia. Prostate stromal cells also express GPR30 and GPER receptors. Their stimulation is caused by an increase in the inflammatory state (mediated by estrogen).

The role of estrogen in the genesis of benign prostatic hyperplasia continues to be studied. Only a few research studies have found a link between elevated estrogen levels or a high estrogen/androgen ratio and benign prostatic hyperplasia.

Benign prostatic hyperplasia, urinary symptoms, and inflammation

Benign prostatic hyperplasia is defined as the hyperproliferation of the stromal component, and to a lesser extent, of the epithelial component of the prostate. That causes the gland to increase in size. Prevalence increases with age, reaching 40-50% of males aged 50-60 and 80-90% of men over 80 years of age.

Although the diagnosis of benign prostatic hyperplasia is histological (tissue sample), a diagnosis of presumption is usually made with the help of clinical data (lower urinary tract symptoms-LUTS) and by examination (digital rectal exam). Benign prostatic hyperplasia may be asymptomatic but the risk of discomfort also increases over time. Prostate growth puts pressure on the urethra and bladder, making it harder to urinate and empty the bladder. In very severe cases, hydronephrosis (reflux to the kidneys and ureteral dilation) may occur.

The prostate is characterized by an organized immunocompetent system that includes lymphocytes, macrophages, and granulocytes (the prostate-associated lymphoid tissue or PALT). A man’s genitourinary system is exposed to different bacterial infections, which can be symptomatic or asymptomatic. The PALT will be activated when there is a prostate infection. Chronic inflammation is accompanied by the secretion of interleukins, present in advanced stages of benign prostatic hyperplasia. This way, chronic infectious stimulus triggers a cascade of immune events that cause hyperplasia in the prostate stroma.

Patients with prostatitis have a greater number of clostridium and bacteroides compared to healthy men (these are predominantly lactobacilli and staphylococcus). This dysbiosis is thought to perpetuate inflammation.

Metabolic disorders

Epidemiological studies have found a link between patients with disorders in their glucose metabolism/hyperinsulinism and benign prostatic hyperplasia. Low HDL cholesterol and high triglyceride levels have also been shown to be associated with larger prostate volumes.

We are talking about associations based on observational studies that serve as the basis for developing hypotheses, but it is true that inflammation is a fundamental element in the genesis of benign prostatic hyperplasia, and this low-grade inflammatory state is typical in individuals with metabolic syndrome. Everything seems to fit.

A hyperestrogenism that is secondary to metabolic disorders (for example, obesity hypogonadism) modifies the ratio between testosterone and estradiol (T/E2), which leads to the expression of different genes in the prostate. A low T/E2 ratio is associated with an increase in the expression of numerous cytokines and markers of cell immunity activation.

Low testosterone

Low testosterone is a risk factor for the development of benign prostatic hyperplasia and urinary system symptoms. The mechanism by which low testosterone promotes BPH is still being studied, but this hormone is known to work by modulating the inflammatory and immune response in prostate tissue (1).

Summary of preventive measures in benign prostatic hyperplasia

The above mentioned mechanisms and pathological hypotheses lead us to make specific recommendations to prevent the development of benign prostatic hyperplasia, namely the following:

1. Treating subclinical/clinical prostate infections (prostatitis)
2. Weight management, avoiding overweight and obesity
3. Maintaining acceptable levels of visceral fat
4. Doing physical activity on a regular basis
5. Management of metabolic disorders (dyslipidemia and insulin resistance/prediabetes/diabetes)
6. Ensuring adequate testosterone levels (diet and hormone replacement under medical supervision).

BIBLIOGRAPHY

(1) Rastrelli G, Vignozzi L, Corona G, Maggi M. Testosterone and Benign Prostatic Hyperplasia. Sex Med Rev. 2019;7(2):259-271. doi:10.1016/j.sxmr.2018.10.006. https://pubmed.ncbi.nlm.nih.gov/30803920/

La entrada Benign Prostatic Hyperplasia (BPH): A Combination of Factors se publicó primero en Neolife.

The physical appearance of hair loss often affects a woman’s mood, worsening her quality of life. A fairly common type of hair loss in women is androgenetic alopecia, also known as female pattern hair loss.

It is characterized by a progressive loss of terminal hair around the front of the head and at the vertex of the scalp. It is important to first diagnose it and then provide adequate therapeutic responses to improve this condition. We discussed androgenetic alopecia in men in our last newsletter; here we will highlight some differences and things that are specific to women with this condition.

Dr. Celia Gonzalo Gleyzes – Neolife Medical Team

Some features of this type of alopecia

Androgenetic alopecia in women or female pattern hair loss (FPHL) is characterized by the progressive loss of terminal hair in the front of the head and at the vertex of the scalp, with a visible reduction in hair density. Compared to men, terminal hair loss is usually incomplete and follows the front line.

The prevalence is lower in Asian women than in Caucasian women.

FPHL may occur after puberty, but it most commonly occurs after menopause.

As in males, the process of miniaturization of the follicle occurs; in the affected areas. we will observe fine hair, of the vellus hair type. The duration of the growth phase (anagen phase) of the hair follicles is reduced, going from a few years to just weeks or months.

Do hormones play a part in all this?

Women with hormonal problems, like hyperandrogenism, that is, who have higher levels of “male hormones” (e.g. polycystic ovary, ovarian hyperthecosis, androgen secreting tumors of the ovaries or adrenal glands) may develop an earlier FPHL. However, most women with FPHL have normal androgen levels.

Theories that explain FPHL include an increased sensitivity of hair follicles to androgens, the influence of estrogens, and genetics (multiple genes involved).

How is FPHL diagnosed?

It is essential to develop a complete medical history in which the patient is asked about things like age of onset, signs of virilization, obstetric background, treatments, use of supplements or hormone therapy, and family history of alopecia.

The scalp will then be examined to identify the distribution pattern and sometimes a trichoscopy (magnified observation) will be performed. Finally, it will be necessary to carry out an analysis with adequate hormonal determinations (1).

Treatment 

The first recommendation is usually topical minoxidil at 5%. It should be applied daily to the affected areas of the scalp. Its effects are visible after 4 months, and the treatment should be continued for at least 12 months, in order to assess the full response. Latanoprost, a prostaglandin analogue and a molecule that improves the oxygenation of the hair follicle, may be incorporated into the formula of this topical solution.

Next, we have spironolactone, an aldosterone antagonist, which competitively blocks the androgen receptor and weakly prevents their synthesis. We usually start with a low dose to check tolerance. Some women may experience headaches, decreased libido, and orthostatic hypotension (low blood pressure), among other symptoms. Combining minoxidil with spironolactone is a good therapeutic recommendation.

Although many women take 1 mg finasteride (a drug that decreases the transition to dihydrotestosterone), the studies conducted do not show good results with this dose, but rather with higher doses or with dutasteride (an administration outside their licensed indication).

Like men, women might resort to other treatments such as platelet-rich plasma (PRP) scalp injections that provide growth factors in large concentrations or low level laser therapy (LLT).

If the problem is chronic and conspicuous, surgery, i.e.hair implants, would be an option to consider (2,3,4).

Once again, we invite women who suspect they suffer from FPHL to consult with a doctor who is able to indicate and supervise treatment, to avoid self-medication and its possible complications.

BIBLIOGRAPHY

(1) Up To Date: Female pattern hair loss (androgenetic alopecia in women), Pathogenesis, clinical features, and diagnosis

(2) Up To Date: Female pattern hair loss (androgenetic alopecia in women): Treatment and prognosis.

(3) https://www.ncbi.nlm.nih.gov/pubmed/30261560 Dermatol Online J.

(4) https://link.springer.com/article/10.1007%2Fs10103-017-2385-5 

La entrada Solutions for Women with Androgenetic Alopecia se publicó primero en Neolife.

Progesterone is becoming one of the most hopeful treatment options for patients suffering from this disease.

Progesterone is one of the “female sexual” hormones secreted by the ovaries; it is fundamentally cyclical, with a secretory peak from day 13-16 of the cycle, and a sharp fall 1-2 days before the menstrual period begins. This hormone is beneficial both in premenopausal women, due to its relief of premenstrual syndrome, and in postmenopausal women, where it balances the proliferative action of estrogen and mitigates symptoms such as headaches, mood swings or insomnia.

Dr. Francisco Martínez Peñalver – Neolife Medical Team

Currently there is research being conducted into some progestogens that may be useful in the battle against breast cancer.

In medicine it is very common for young doctors to inherit “dogmas of faith” from our teachers – red lines that should never be crossed, and that serve as a basis on which to build the rest of our knowledge.

Very occasionally this knowledge, that is accepted without doubt, is proven wrong by the scientific literature. A small earthquake occurs in the medical world, since it involves changing some of the main principles that govern our daily practice and our medical knowledge.

To this we should add that as technology advances we are becoming more aware that in the human body there is little “bipartisanship”, there is little “black or white”. The samemolecule, the same cell, in different locations, even at different times, acts in a totally opposite way. The basis of all this is the adaptive mechanism that for thousands of years has been modeling the human being, seeking to turn it into a perfect machine capable of acclimatizing to the different circumstances that are going to affect it in the process of living.

One of these paradigms of medicine that is currently close to being torn down is that of Progesterone. Progesterone is one of the “female sexual” hormonessecreted by the ovaries; it is fundamentally cyclical, with a secretory peak from day 13-16 of the cycle, and a sharp fall 1-2 days before the menstrual period begins.

Between the early 1990s and 2002, virtually all the literature produced about hormone replacement therapy was based on the largest epidemiological study ever conducted, the WHI (Women’s Health Initiative ) (1). The conclusions published by this study from 1989 to 2002 were devastatingly against hormone therapy . Not only did the incidence of cardiovascular events increase, but the incidence of breast cancerand cancer of the uterus increased exponentially in the patients who underwent the therapy.

Over the years, however, cracks have appeared in these conclusions. The two fundamental ones were that the WHI patients had had more than 10 years since the beginning of the menopause and that those 10 years without protection from theirestrogen already justified the increase in cardiovascular mortality; and a second failure – this much more important – where it was demonstrated that the progesterone analogue administered, Medroxyprogesterone Acetate , not only did not exercise the beneficial actions of progesterone, but that it produced an “excess estrogenic effect”, which is dangerous tohealth. That is to say, that the participants of the study did not represent the population in a truthful manner, and that what was given as an analog to progesterone had the opposite effects (2).

However, whereas the WHI results against the use of hormone replacement therapywere published with a great fanfare in all the newspapers and were front-page news, the news that came after and that annulled the results of the WHI has not been given much attention by the press in general (3).

For all these reasons, the image we have of a drug such as Progesterone is pernicious, and a dark legend has been generated around its use that we doctors who dedicate ourselves to Bioidentical Hormone Replacement Therapy need to disassemble.

To begin with this demystification, we need to take a look at a review of clinical studies published in January 2017 in the journal Nature Reviews Cancer (4). According to this article by directors Carroll and Hickey, the term progestogenshas been used generically to refer to a series of compounds that activate the progesterone receptors and the term progestins for molecules that mimic the activity of progesterone. Progestins, apart from the progesterone functions, have other actions that may increase the risk of breast cancer; hence the confusion. However, there is no study that even suggests the possibility that progesterone can cause breast cancer. Nevertheless, there is indeed currently research being conducted into some progestogens that may be useful in the battle against breast cancer. The conclusions of this article are that progestogens have a beneficial effect in those estrogen-dependent tumors in combination with the new drugs that block these estrogen receptors. In fact, there is a clinical trial under way for breast cancer patients withestrogenic receptors and positiveprogesteronics, in this case with progesterone (5).

Therefore, progesterone is now changing from playing a harmful role with a dark legend behind it, to being one of the most hopeful treatment pathways for patientssuffering from this disease.

At Neolife, according to the most recent scientific evidence, for a long time we have been taking advantage of the benefits of this hormone, progesterone, both in premenopausal women – for the relief of premenstrual syndrome – and in postmenopausal women -where it balances the proliferative action of estrogen and mitigates symptoms such as headaches, mood swings or insomnia.

BIBLIOGRAPHY

(1) https://www.whi.org/about/SitePages/About%20WHI.aspx. WHI website.

(2) Speroff L. Am J Obstet Gynecol. 2003 Sep;189(3):620

(3) Harman SM et al. Is the estrogen controversy over? Deconstructing the Women´s Health Initiative study: a critical evaluation of the evidence. Ann N Y Acad Sci 2005 Jun; 1052:43-56.

(4) Carroll JS Hickey TE. Deciphering the divergent roles of progestogens in breast cancer. Nat Rev Cancer. 2017 Jan;17(1):54-64.

(5) ISRCTN – ISRCTN23662758: A trial looking at progesterone to treat early breast cancer in premenopausal women.

La entrada Progesterone: from villain to hero hormone in breast cancer se publicó primero en Neolife.

A study in the journal Jama Psychiatry demonstrates how hormone therapy may prevent the depressive symptoms that often appear during menopause.

In addition, an article published in the journal Menopause highlights among its conclusions how oestrogen deficiency in women acts as a catalyst in the equation “depression is equal to compulsive eating and obesity”. However, the intimate physiopathological mechanisms regulating this equation, are for the moment, still unknown.

Dr. Moisés De Vicente – Neolife Medical Team

A study published in the journal Jama Psychiatry demonstrates how hormone therapy may prevent the depressive symptoms that often appear during menopause.

Weight gain is an issue that the majority of people must face as they enter their 50s. As is well known, obesity (defined as having a body mass index greater than 30) increases the chances of developing insulin resistance and, consequently, the onset of insulin-related diseases, such as metabolic syndrome, diabetes and cardiovascular diseases.

There are many reasons behind such developments, most of which depend on a number of factors. First and foremost, on our habits and lifestyle, which we will have often developed (for better or worse) during our childhood and youth. However, there are other associated factors, such as genetic factors and factors associated with other comorbidities that can push us down the path of weight gain.

Women, at this age, present an even greater risk than men of suffering weight gain and even obesity. Several studies have described how up to 40% of women over 40 are in fact obese or are overweight¹. There is a fundamental factor in the development of this situation within this demographic: the menopause transition.

However, there is an other important factor, and one which must be taken into account in the development of weight gain, and that is depression^{2, 3}, or at the very least, the presence of depressive symptoms. Depressive symptoms are frequently present during the menopause transition. During menopause, influencing factors not only include the decline in oestrogen levels, but also the type of society in which, unfortunately, we still live in.

The relationship between compulsive eating, the presence of depression, and obesity has been covered in multiple articles⁴. Thus, the vicious circle of menopause, depression, compulsive eating and obesity is complete. In fact, in many cases it is impossible to determine what came first: I’m feeling depressed due to the decline of oestrogen production, so I’m eating more and eating worse foods (mainly foods with a high caloric intake) or, I’m eating more due to my lifestyle, which reduces oestrogen production and consequently I’m feeling depressed, etc.

This association has recently been demonstrated in an article published in the journal Menopause⁵. It highlights among its conclusions how oestrogen deficiency in women acts as a catalyst in the equation “depression is equal to compulsive eating and obesity”. However, the intimate physiopathological mechanisms regulating this equation, are for the moment, still unknown.

In view of this cycle in which we find ourselves, numerous nutritional, behavioural, and even anti-depressant therapies have been suggested in order to break this vicious circle. Nevertheless, the failure rate of these therapies is high. On their own, behavioural and nutritional therapies fail to reduce the feelings of unease and anxiety that compulsive eating often produces. They can help to control weight, though in many cases only temporarily, thanks to a strong discipline that sooner or later the patient is no longer able to maintain, inevitably succumbing to the impulse to binge.

On the other hand, antidepressant treatments can prove to be more successful in the long term. However, many of these present weight gain as a side-effect, thus failing to break the spell. Though as a lesser of two evils, they allow for a much more gradual weight gain which in many cases improves the associated depressive symptoms.

So what is there to do? Should women just succumb to depression and food once they reach a certain age? A study has recently been published in the journal Jama Psychiatry⁶ which demonstrates how hormone therapy can prevent the depressive symptoms that appear during this stage of the menopause transition. The article explains how patients undergoing oestrogen treatment with transdermal oestradiol (different brands where used) and intermittent micronized progesterone, developed less depressive symptoms compared to women who had received placebo. In fact, benefits were greater in women who had suffered from stressful life events and those who began treatment in the early stages of the transition.

It should be noted that these results remained significant even after adjusting statistically for the presence of vasomotor symptoms. That is, hormone treatment contributes directly to preventive benefits on your emotional state, independently of its beneficial effects on the symptoms of menopause.

Today, hormone replacement therapy is achieving numerous beneficial effects for countless patients. At Neolife, we use this type of treatment to alleviate the symptoms associated with menopause. With this therapy, not only can we improve your hormonal situation, but also improve your emotional state and prevent the possible development of other types of diseases or comorbidities, such as in this case, obesity.

BIBLIOGRAPHY

(1) Ogden C, Carroll M, Fryar C, Flegal K. Prevalence of obesity among adults and youth: United States. NCHS Data Brief 2015; 219:1–8.

(2) Simon G, Ludman E, Linde J, et al. Association between obesity and depression in middle-aged women. Gen Hosp Psychiatry 2008; 30:32–39.

(3) Jasienska G, Ziomkiewicz A, Górkiewicz M, Pajak A. Body mass, depressive symptoms and menopausal status: an examination of the “Jolly Fat” hypothesis. Womens Health Iss 2005; 15:145–151.

(4) Konttinen H, Manniesto S, Sarlio-Lahteenkorva S, Silventoinen K, Haukkala A. Emotional eating, depressive symptoms and self-reported food consumption: a population-based study. Appetite 2010; 54:473–479.

(5) Dana R. Schreiber, MS and Natalie D. Dautovich, PhD. Depressive Symptoms and Weight in Midlife Women: The Role of Stress Eating and Menopause Status. 2017; 24(10):1190-1199.

(6) Jennifer L. Gordon, PhD1; David R. Rubinow, MD2; Tory A. Eisenlohr-Moul, PhD2; et al. Efficacy of Transdermal Estradiol and Micronized Progesterone in the Prevention of Depressive Symptoms in the Menopause Transition. A Randomized Clinical Trial.

La entrada How to kill “three” birds with one stone: depression, obesity and menopause se publicó primero en Neolife.

Bioidentical testosterone therapy, at the right doses, is completely safe and allows for a correct hormonal restoration. Nevertheless, myths and rumours still circulate despite lacking any scientific evidence.

Some of the misconceptions that abound in the collective imagination are: that testosterone is a “male” hormone; that its only role in women is for sexual desire and libido; that replacement therapy makes women more masculine; that it gives you a deeper (more manly) voice; that it causes hair loss; that it can have adverse side-effects on your cardiovascular system; that it causes aggression; or that it can increase the risk of breast cancer.

Dr. Iván Moreno – Neolife Medical Team

Many of these myths that create such a bad reputation for hormones are in fact extrapolations of the adverse effects seen from taking very high doses of anabolics, which have nothing to do with bioidentical testosterone.

Testosterone therapy is being increasingly used to alleviate symptoms of hormonal deficiency in pre and postmenopausal women.

Although numerous scientific studies show the safety and success of this treatment, rumours and myths have been created, which by sheer force of repetition seem to hold more “influence” despite lacking any supporting medical evidence.

Many of these myths are extrapolations of the adverse effects seen from taking very high doses of anabolics (testosterone derivatives) for other purposes (such as bodybuilding, doping, etc.).

In this article, we refer solely to therapy with bioidentical testosterone (which is identical to a human testosterone molecule) and only at replacement doses which aim to replenish the physiological levels we already had in our youth; this is the standard that governs a correct hormone restoration, which we employ here at Neolife.

Myth 1: Testosterone is a “male” hormone.

While it is true that men have higher levels of testosterone, the most abundant sex hormone present in a women’s body is also testosterone. Oestrogen (typically referred to as the “female” hormone), although present throughout a women’s life, is found in concentrations 10 times lower than that of testosterone. Testosterone, in balance with lower doses of oestradiol, is equally important for both sexes.

Fact: testosterone is the most abundant and biologically active hormone in women.

Myth 2: The only role of testosterone in women is for sexual desire and libido.

Another misconception, given that testosterone receptors are found in practically all tissues of a women’s body. Testosterone and its precursors decrease with age, and pre and postmenopausal women may experience symptoms of androgen deficiency such as: mood disorders, lack of well-being, fatigue, loss of bone density and muscle mass, mental dullness, memory disorders, hot flushes, joint discomfort, and sexual dysfunction etc.

Fact: testosterone is essential to a woman’s physical and mental health.

Myth 3: Testosterone treatment makes women more masculine.

Restoring a woman’s ideal hormone levels (to that which we had between the ages of 18-25 years old) far from making you more masculine, can in fact make you more feminine. Treatment should not be confused with the high supra-pharmacological doses which are administered to patients requiring more drastic changes due to gender issues; in which case, symptoms are still reversible by merely reducing the dosage.

Fact: excluding supra-pharmacological doses, testosterone has no masculinizing effects on women.

Myth 4: Testosterone will make your voice deeper (more masculine).

Hoarseness of voice can affect us at different times due to inflammation or infection of the throat, but is always reversible. There is no procedure whereby testosterone could produce such a phenomenon; even in cases of high doses of other androgens, there is no clear evidence of producing a deeper voice or any irreversible changes to the vocal chords.

Fact: there is no evidence that testosterone changes your voice.

Myth 5: Testosterone causes hair loss.

Hair loss is a complex and multifactorial process which is also genetically determined. “Androgenic” alopecia refers to the similar type of pattern baldness commonly found in men, not referring to the cause, but rather to the defined pattern. In any case, it is dihydrotestosterone (DHT), and not testosterone, which is involved. Obesity and insulin resistance, as well as alcohol, a sedentary lifestyle and some medications, can increase the conversion of testosterone to DHT and oestradiol in the hair follicle.

Approximately one third of women experience brittle hair and hair loss with age, which often coincides with a decrease in testosterone levels. However, there are studies in which hair regrowth has been achieved due to subcutaneous testosterone implants in such women.

Fact: testosterone does not cause hair loss; in fact, in some cases it can improve hair regrowth.

Myth 6: Testosterone has adverse effects at a cardiovascular level.

Unlike synthetic anabolics, there is no evidence that testosterone has any adverse effect at a cardiovascular level. In fact, its replacement has a beneficial effect on the metabolism of glucose and lipids, as well as on the maintenance of “lean mass” in both men and women’s bodies.

The most complete meta-analysis ³ carried out on this topic shows that there is no greater cardiovascular risk with testosterone replacement therapy; in fact, a lower occurrence of cardiovascular disease has been demonstrated in some groups (those presenting a higher cardiometabolic risk).

Fact: there is substantial evidence supporting the cardiovascular safety of testosterone, which even indicates a likely protective effect.

Myth 7: Testosterone damages the liver and can cause “clotting” (venous thromboembolic disease).

This is an “imported” rumour from the world of anabolic (synthetic androgens) over-use, which when taken orally in high doses, can in effect, cause liver damage. The truth is that parenteral testosterone (gels, skin patches or subcutaneous implants) avoids that first step through the liver and thus has no adverse effects (i.e. there is no increase in transaminase enzymes nor any alteration to the factors that affect blood clotting). There is therefore no relationship between testosterone administered in this way and the occurrence of blood clots (thrombosis, embolism), unlike synthetic steroids, or oestrogens taken without progesterone and progestins.

Fact: non-oral testosterone does not damage the liver or increase blood clotting.

Myth 8: Testosterone causes aggression.

Although the use of anabolics at high doses can cause aggression and attacks of “rage” (hence the rumour), this does not happen with testosterone. Even with supra-pharmacological doses of intramuscular testosterone, there has been no clear onset of aggression.

As has been previously mentioned, in cases of obesity, alcohol consumption, or a marked sedentary lifestyle, the conversion rate of testosterone to oestradiol can be seen to increase. The effects of excess oestrogen (oestradiol and its derivatives) however, have been associated with irritability and aggression in other species. In fact, in women presenting symptoms of androgen deficiency, treatment with testosterone has been shown to improve anxiety and irritability in more than 90% of cases².

Fact: testosterone therapy is not linked to aggression; even in women suffering from testosterone deficiency, therapy improves anxiety and irritability.

Myth 9: Testosterone may increase the risk of breast cancer.

Since 1937, it has been known that the development of breast cancer is usually dependent on oestrogen. Testosterone, however, could play a possible role in slowing down the growth of breast tissue, and may even be a treatment for breast cancer.

In recent studies, in which testosterone was administered together with an aromatase inhibitor (preventing any conversion into oestrogen), they found the tumour to reduce or even disappear⁵.

Fact: testosterone does not increase chances of breast cancer; in fact, it could help to prevent it.

Myth 10: the safety of testosterone use in women has not been tested.

Data of treatment at very high doses in transgender patients has existed for more than 40 years, and has shown this treatment to be safe. Any side-effects have been the consequence of oral intake (which is no longer used) or due to the conversion to oestradiol (which is rarely a problem at the doses used for bioidentical hormone replacement).

Fact: the safety of non-oral testosterone use has been well established in women for cases of very long-term treatments.

BIBLIOGRAPHY

(1) Glaser, R., & Dimitrakakis, C. (2013). Testosterone therapy in women: myths and misconceptions. Maturitas, 74(3), 230–234.

(2) Glaser R, York AE, Dimitrakakis C. Beneficial effects of testosterone therapy in women measured by the validated Menopause Rating Scale (MRS). Maturitas 2011; 68: 355–61.

(3) Corona G, Rastrelli G, Maggi M. Diagnosis and treatment of late onset hypogonadism: systematic review and meta- analysis of TRT outcomes. Best Pract Res Clin Endocrinol Metab 2013; 27: 557-579.

(4) Hackett, G., Kirby, M., Edwards, D., Jones, T. H., Wylie, K., Ossei-Gerning, N., et al. (2017). British Society for Sexual Medicine Guidelines on Adult Testosterone Deficiency, With Statements for UK Practice. The Journal of Sexual Medicine, 14(12), 1504–1523.

(5) Glaser, R., & Dimitrakakis, C. 2015. Testosterone and breast cancer prevention. Maturitas, 82(3), 291–295.

La entrada 10 myths about testosterone treatment in women se publicó primero en Neolife.

Oestrogen improves the cardiovascular risk profile of male patients.

In men, oestrogen has a beneficial effect on bone metabolism, preventing the appearance of osteoporosis and contributing to the ageing of the joints during pubertal development. At a cardiovascular level, oestrogen in men has also been found to increase the level of “good cholesterol”, c-HDL.

That is to say, oestrogen contributes, in part at least, to delaying the appearance of atheromatous plaque that may later cause cardiovascular events. In addition, oestrogen enhances insulin function (reducing glycemia), regulates appetite, energy expenditure, and as a consequence of this can be deemed detrimental to an individuals body weight.

Dr. Francisco Martínez Peñalver – Neolife Medical Team

Oestrogen is responsible for the difference between women and men in terms of cardiovascular health.

Within medical literature there remain a number of controversies which must be clarified including biomarkers which have been subject to uncertain interpretations, substances that appear to be harmful but turn out to be beneficial to the patient, and treatments that are reviled for a long time but due to the passage of time have been re-discovered and now represent an advancement in a specific medical discipline.

Normally, when we talk about oestrogen it is in relation to the effect the hormone is known to have on the different stages of a woman’s life. This perspective is not however the subject of this article, but by way of a brief summary we will explain that oestrogen in women provides a clear example of how a specific type of therapy which is beneficial when applied by trained doctors may ultimately fall into disuse due to an unfounded poor reputation. Oestrogen is responsible for the difference between women and men in terms of cardiovascular health, notwithstanding that all feminine traits are similarly nourished by the same hormones. After the menopause, the production of oestrogen ceases and the statistics relating to cardiovascular death in men and women are comparatively similar over the subsequent years, which is accompanied with a decline in feminine features and attributes (the chest loses smoothness, vaginal dryness appears, urinary incontinence, loss of libido etc.). The use of oestrogen-like substances, not the bioidentical hormone itself however, has led to the occurrence of certain side effects amongst patients that have been attributed to bioidentical oestradiol, but which are actually produced by substances similar but not identical to the substances themselves. In the heat of battle, oestrogen replacement therapy with oestrogen has fallen into disuse broadly condemning woman to suffer symptoms associated with the onset of the menopause that could be avoided without undue risk.

Until a few decades ago there was no medical research on the effect of oestrogen in men. It may be necessary to explain here that men also produce oestrogen, in the testes, and that testosterone itself is produced by peripheral tissues, thanks to an enzyme called “aromatase”. The principal sites where this enzyme is shown to have a considerable effect is in fatty tissues, the liver and skin.

In men, oestrogen has a beneficial effect on bone metabolism, preventing the appearance of osteoporosis (1), and contributing to the ageing of the joints during pubertal development. At a cardiovascular level, oestrogen in men has also been found to increase the level of “good cholesterol”, c-HDL. That is to say, oestrogen contributes, in part at least, to delaying the appearance of atheromatous plaque that may later cause cardiovascular events. Oestrogen has a relaxing effect on the wall of the arteries, in particular the coronary arteries, which helps to prevent the formation of atheromatous plaque at that level. In addition, oestrogen enhances insulin function by reducing glycemia. And this aspect is important because by enhancing insulin function we are able to prevent the accumulation of visceral fat. In addition, oestrogen regulates appetite (through leptin pathways at a brain level), energy expenditure, and as a consequence of this oestrogen remains a determining factor in terms of an individuals body weight (2), since oestrogen also prevents the development of pre-adipocytes and the secretion of cortisol. Therefore, oestrogen improves the cardiovascular risk profile of male patients.

But as is the case for women, there are some controversies which persist in the world of medicine about the positive effects that we have just described and have been fully demonstrated. Men who have defective oestrogen receptors commonly suffer from insulin resistance, visceral fat gain, and interestingly, an increase in oestrogen levels as the body attempts to resolve the situation. This situation can never be achieved because the receptors are insufficient or deficient.

If we now return to the reason for the controversy – it is that in those patients with excess visceral fat, we usually find increased levels of oestrogen. On this particular point, there are two possible explanations. The first is a theory that existed a few years ago, which proposes that visceral fat has transformed into oestrogen and this in turn creates a vicious circle of fat gain and ever decreasing levels of testosterone that leads the patient to lose quality of life as well as shorten their lifespan.

However, there is data from a recent study which illustrates that testosterone is converted into oestrogen in visceral fat, which suggests that this helps to decrease insulin resistance (which prevents the dissolution of such fat) and reduce the abdominal circumference. In those patients with poor or deficient oestrogen receptors (and this depends on the genetic makeup of the patient concerned), the production of oestrogen will be increased in an attempt to compensate for said deficiencies but this does not mean that oestrogen is to blame for the patient’s weight gain. In summary, if we refer to the age old question of which came first the chicken or the egg, it is necessary to answer as follows: the elevated oestrogen levels found in patients with a high visceral fat index which has been caused by a failure in the oestrogen receptors (3), can be explained by reference to the body’s reaction when the body first detects that there is an increase in insulin resistance due to the excess visceral fat and overproduces said oestrogen in an attempt to fix the situation. This excess visceral fat produces pro-inflammatory factors that are part of the harmful characteristics discussed previously and that can encourage the appearance of vascular diseases and some types of cancer.

On the other hand, and this is known and proven to be the case, the excess oestrogen is harmful to the production of testosterone in the testicles and this affects vital functions in the man, such as muscular capacity, energy and of course the presence of sexual desire. Therefore, once again, one should look for the correct endocrine balance so that all functions and all aspects of health dependent on this complicated balance are maintained in a balanced equilibrium.

At Neolife, we take a comprehensive approach to the patient as we believe that it is necessary to take into account, amongst other factors, the hormonal balance of the patient. By using our densitometry we are able to measure the levels of visceral fat in the patient. We also use the blood levels to help us determine the different hormones which can be used as part of a review of the physical activities undertaken by the patient such as their eating habits, etc. This allows us to establish a personalised plan to ensure that the patient can successfully implement the changes necessary to balance quality of life with proactive measures to prevent future health problems.

BIBLIOGRAPHY

(1) Ornstrup MJ1et al. Eur J Endocrinol. 2015 Feb;172(2):205-16. Adipose tissue, estradiol levels, and bone health in obese men with metabolic syndrome. (2) Rubinow KB1. Estrogens and Body Weight Regulation in Men. Adv Exp Med Biol. 2017;1043:285-313 (3) Ismail I, Keating SE, Baker MK, Johnson. A systematic review and meta-analysis of the effect of aerobic vs. resistance exercise training on visceral fat. NA.Obes Rev. 2012 Jan;13(1):68-91

La entrada The importance of oestrogen for men se publicó primero en Neolife.

The excellent nutritional quality of seeds makes them essential to maintaining a varied, healthy and balanced diet.

Flax seeds are one of the best dietary sources of soluble fibre. Hemp seeds offer a mega-dose of magnesium and a beneficial ratio of omega 3/omega 6 fatty acids. And sunflower seeds provide an impressive source of unsaturated fats and minerals such as iron, magnesium, copper and manganese, as well as an excellent source of vitamin E.

Tania Mesa – Nutritionist and Nurse from Neolife

The seeds: unknown in the kitchen, but full of vitamins, minerals, fibre, essential oils…

Although they were widely known and used in the past, we have allowed seeds to drift into obscurity. Their names are known to us, but we do not know what they can provide to our diet or how they can be added to our daily diet?

In our personal and professional experience seeds are essential to maintaining a varied, healthy and balanced diet: they are a vital source of fibre, vitamins, omega 3 and 6, proteins and minerals, whilst helping to increase the level of “good” HDL cholesterol and decrease the “bad” LDL cholesterol, improving intestinal transit, satiety (fullness) and helping us to maintain weight etc.

Once the seeds are exposed to heat, the vitamins, minerals and their essential oil profiles become denatured. In order to absorb the nutrients contained within the seeds, they must be consumed in their natural form, that is to say raw.

However, do not think that the fact that they can not be subjected to heat means that they can not be soaked, ground or pureed.

Next we outline the healthiest seeds. All of the seeds stand out for their excellent nutritional characteristics and should, therefore, be added to your diet:

Flax seeds

Flax is one of the best dietary sources of soluble fibre. They help slow digestion, reduce cholesterol levels and regulate blood sugar and appetite (therefore, it is ideal for weight loss).

They are well-known for their fibre content, but also for their high levels of omega 3 alpha-linolenic acid (ALA) and antioxidants. For this reason they also help decrease the production of agents in the body that promote inflammation and levels of the C-reactive protein (CRP) in the blood, a biomarker for inflammation that we have measured recurrently at Neolife. They also contain lignans, which are phytoestrogens, plant compounds that have oestrogen-like effects and antioxidant properties that help stabilise hormone levels, reduce the symptoms of premenstrual syndrome and the menopause; they can also help maintain blood pressure levels and, consequently, decrease the risk of cardiovascular disease.

Be sure to use ground flax seeds, as whole seeds pass through the digestive tract without providing any nutrients. This is because the flax seed has a hard outer shell that makes it hard to break. You should keep this in mind if you eat bread or one of those cereal products which contain whole flax seeds.

However, flax seeds last longer if purchased whole; as they can always be ground up in a coffee grinder or with a spice blender for consumption. However, if you buy pre-packaged flax, you should store the seeds in the refrigerator or freezer to maintain their freshness.

In the kitchen: sprinkle them on any food, including salads, post-workout shakes, hot cereals, yoghurts, baked vegetables, as an egg substitute or even include them in homemade pastries.

Hemp seeds

Hemp seeds offer a mega-dose of magnesium, which regulates muscle/nerve function, blood sugar and blood pressure; furthermore, they have a beneficial omega 3 / omega 6 fatty acid ratio, (3:1 ratio), which helps maintain good heart health. On the other hand, eating hemp seeds adds a nice nutty flavour and smooth texture to food.

In the kitchen: mix into smoothies, soups and salads.

Sunflower seeds

They are an impressive source of unsaturated fats and minerals such as iron, magnesium, copper and manganese. They are also an excellent source of vitamin E, the body’s main fat-soluble antioxidant, which help improve exercise recovery by reducing the oxidative stress induced by training. In addition, sesame seeds have one of the highest phytosterols content levels, which are present in plant compounds that have a chemical structure very similar to that of cholesterol and that when present in sufficient quantities in a diet can be used to reduce blood cholesterol levels.

In the kitchen: can be consumed in all kinds of ways. They can be added to salads, yoghurts, shakes or mixed into sauces. If you make your own bread, biscuits or homemade buns, you can dip the top in sunflower seeds before baking.

In the following blog we will talk about the properties of sesame seeds, pumpkin seeds, chia seeds and quinoa.

La entrada Small, but excellent allies in our diet (1) se publicó primero en Neolife.

A new guide published by the British National Health Service has recognized the virtues of Hormone Replacement Therapy.

The publication has received widespread media coverage in the United Kingdom, as shown by the two articles published in The Guardian in November last year. This repositioning of official medicine is gradually approaching the position and approach proposed by Age Management Medicine (or Preventive Anti-ageing Medicine).

Neolife medical management

The national public healthcare system reviews your views on the menopause and hormone replacement therapy.

In November 2015 news broke that had socio-health implications for the controversial hormone replacement therapy (HRT) and the menopause. This is the first guide on the subject published by the British National Health Service (National Institute for Health and Care Excellence-Nice). The objective of this document is to provide physicians with updated information based on the latest scientific literature and also to inform patients to take part in the decision about how they should be treated.

The publication of this guide had a widespread impact in the United Kingdom, as can be seen in some articles published in The Guardian:

• HRT could benefit one million women, says NHS menopause guidance (HRT could benefit one million women, according to the new guide on the menopause produced by the British National Health Service).
• HRT opened my eyes, and gave me my life back (“HRT opened my eyes and restored my life”).

In Spain the average age of the menopause is around 51 years old and it is estimated that there are between 1 and 3 million women with symptoms which include night sweats, hot flushes, lack of drive (lethargy), fluctuations in mood, decreased libido, etc. For some women these symptoms can seriously affect their quality of life and usually last for about 4-5 years. As a result hormone replacement therapy is the appropriate treatment to combat the above symptoms.

Hormone replacement therapy for the treatment of menopause began in the 1960s and quickly became popular in developed countries. For socio-political reasons in Spain, this happened much later. At the beginning of the 21st century some results were published from a couple of large clinical studies that demonstrated links between hormone replacement therapy and cardiovascular disease, brain thrombosis and breast cancer. These studies were the WHI (Womens Health Initiative), which was published in the USA in 2002, and the Million Women Study, which was conducted in the United Kingdom and published in 2003. A scandal was generated and the press coverage caused panic and concern about these results and millions of women stopped receiving treatment for symptoms acting under their own initiative and/or on the recommendation of their doctors.

It has been 15 years and things have finally returned to their original course. Properly prescribed and monitored hormone replacement therapy is beneficial for women’s health and their quality of life. We have already discussed this in the Neolife blog on several occasions:

• Hormone balance may reduce some of the most common cancers
• Hormone therapy in women, is it safe?
• X European Congress on the Menopause and Andropause

After multiple commentators criticized the studies and voiced concerns regarding HRT in 2002 and 2003, “mainstream medicine” must now re-position itself in favor of HRT.

Many commentators have criticized the studies:

• For example, in the WHI study pregnant mare estrogen (conjugated equine estrogen) and medroxyprogesterone acetate were used instead of the woman’s natural hormones (17 beta estradiol and progesterone)
• In addition, the average age of the women in the study was 62 years old (13 years after the menopause on average), many of them overweight, obese (34%), hypertensive (36%) and smokers. When the study was reinterpreted by analyzing the results from the youngest women in the study (those under 60 years of age), it was found that there was insufficient evidence to support an increase in cardiovascular risk.
• The increased risk relating to breast cancer was directly linked to the use of a synthetic progestogen, medroxyprogesterone rather than the natural female hormone progesterone.
• The increased risk relating to thromboembolisms was associated only with orally taken estrogen (not transdermally, mucosally or subcutaneously) in women over 60 years of age who also presented with other cardiovascular risk factors, such as smoking and obesity.
• Interestingly, the same study showed a significant reduction in hip and spine fractures in those who suffer from osteoporosis and a lower incidence of colon and rectal cancer, but these beneficial effects were not disclosed…

The new NICE guidelines (National Institute for Health and Care Excellence), the equivalent of the Spanish INS, reflects the “official” positioning of British public healthcare system, which is approaching the position of Age Management Medicine, and distances itself from the position which had previously opposed HRT. Little by little “mainstream medicine” (the official medicine) will have no choice but to acknowledge the scientifically proven benefits of HRT, as well as recognize that the side effects attributed in the original studies were related to a inappropriate prescription of molecules similar to the natural hormones, but not identical. Furthermore, HRT is not limited to the treatment of menopause: it is a complete preventive therapy for both women and men. And it is not just limited to estrogen and progesterone: there is also testosterone, DHEA or melatonin, among other beneficial hormones which can be used.

The British public healthcare system is very similar to the Spanish system and both are of a high quality which rely on protocols and interventionist-style medicine. But the British population, because of their close-relationship to the Americans, is more informed about the demands of American society and therefore they will be the first Europeans to massively demand HRT be made available to all, as is already occurring in the US. Spaniards, particularly Spanish menopausal women, will still have to suffer the deterioration in their quality of life and health for a few more years until our health authorities show a willingness to advance with science in this regard. And all this despite the fact that SEGO (the Spanish Society of Gynecology and Obstetrics) openly criticized the aforementioned studies which took place in 2002 and 2003 back in 2008.

At Neolife we ​​recommend hormone replacement therapy, as long as it is properly prescribed and monitored.

At Neolife we inform our patients of the benefits and possible risks associated with Hormone Replacement Therapy taking into account their personal characteristics (age, cardiovascular risk, poor habits…) and we value the different forms of administration (gels, pellets, tablets etc.) to successfully personalize the treatment to each patient. We always use bioidentical hormones. In addition, we require a complete gynecological study (mammography, cytology and ultrasound) with in the last 9 months and we regularly monitor the development of symptoms, as well as the plasma levels of different hormones in the body.

La entrada Favorable Winds for the Hormonal Treatment of the Menopause se publicó primero en Neolife.

Breast cancer is the most common form of cancer among women, accounting for almost a quarter of all tumors occurring in women with an incidence of 93.6 cases per 100,000 women/year.

The incidence of breast cancer in women is rising between 2-3% each year; among the possible causes of this increase are the changes in reproductive patterns, poor lifestyle habits and hormone replacement therapy with non-bioidentical estrogen and progesterone.

Fortunately, the mortality rate of breast cancer has dropped concurrently with the increase in incidence, thanks to early diagnosis and improved treatments whereby Multidisciplinary Care of breast cancer has played a vital role. In Spain, the overall survival rate from breast cancer currently stands at 83%, which is between 90% in the United States and 79% in Europe.

MAIN RISK FACTORS OF BREAST CANCER

Hormonal and reproductive factors. This includes all situations that involve the breasts being subject to high levels of estrogen throughout one’s life.

• Early menarche (1st menstruation before 11 years old) or late menopause (after 55 years old).
• Nulliparity (never having given birth).
• Late age having 1st child, above 30 years old; can result in a delay in the maturity of the mammary gland.
• Oral contraceptives in young women; excess risk disappears once the treatment is stopped, so the overall effect is scarce.
• Combined hormone replacement therapy.

 Family history.

• Only 15% of cases of breast cancer are associated with family history; and only 5% are associated with a known genetic mutation (BRCA 1 and 2).

 Prenatal risk factors, due to the effect of hormonal exposure in the womb.

• Baby birth weight.
• Advanced maternal age.

Obesity

• It is more significant during post-menopause as the source of hormones comes from adipose tissue.

Diet

• Fundamentally owing to the consumption of alcohol, sugar and fast absorption carbohydrates, as well as polyunsaturated fatty acids and trans fats from hydrogenated oils.

Environmental and occupational factors:

• Ionizing radiation, if exposure has occurred during the first years of life, adolescence or pregnancy. For example, due to thoracic radiotherapy, for diseases such as lymphoma during childhood and youth.
• Women with career changes or night shifts. Changes to the circadian rhythm can involve a decrease or suppression in the secretion of melatonin; this theory is still limited with regards to humans, although it is supported by studies with laboratory animals.

High mammographic density.

Previous breast pathology

• Proliferative lesions with atypia, ductal carcinoma in situ and lobular carcinoma in situ.

BREAST CANCER PREVENTION

Primary prevention 

This involves all of the interventions we can carry out in order to reduce the personal risk of developing breast cancer before it appears.

There is a group of risk factors that can’t be changed and that we can do little to influence:

• Age of menarche and menopause.
• Ionizing radiation treatment for disease before the age of 25.
• The risk of benign breast lesions.
• Family history.

However, other risk factors can be clearly influenced in order to reduce the risks of developing breast cancer:

• Physical exercise. Moderate physical exercise equivalent to walking at a brisk pace 30 minutes a day OR 1 hour a day 3 days a week is enough; it has also been seen to improve the prognosis and favor an improved treatment tolerance in women who have already had breast cancer.
• Diet
  • Decrease maximum alcohol intake to 1 drink a day, especially distilled alcoholic drinks.
  • Reduce the intake of animal fats (from red meat) and polyunsaturated fatty acids and trans fats (margarine, commercial bakery products).
  • A diet rich in fiber, such as vegetables, legumes, fruit, fish and olive oil (the Mediterranean Diet).
  • The consumption of soybean derivatives has not been shown to be of any benefit (except in those of East Asian heritage who may have consumed larger quantities of soybean derivatives from childhood).

• Nutritional supplementation. Sufficient intake of Vitamin D, as this has been shown to inhibit the growth of tumor cells in experimental studies.
• It is difficult to modify the advancement of childbearing age and number of children per woman, as government policies on family protection are influencing factors.

Secondary prevention

Here, the objective is the early diagnosis of the disease in order to be able to perform less aggressive treatments and improve the overall prognosis.

With breast cancer, the only diagnostic test that has proven to reduce mortality rates, by performing it on the public, is screening with mammograms.

When screening campaigns are carried out on the public, they are aimed at women between 50-70 years old, with a screening every 2 years.

They can also be performed as a form of early diagnosis, as part of a gynecological check-up of healthy women starting at the age of 40, although these must take into account the limitations due to the higher radiation density of the breast and the different behavior of tumors in younger women.

In women under 40, an increased risk is only present on a case by case basis owing to both family and personal medical history.

BIBLIOGRAPHY

(1) Epidemiological situation of breast cancer in Spain. Pollán M et al. Psycho-Oncology. Vol 4, num. 2-3, 2007, pp 231-248.

(2) Breast cancer today. Advances in the epidemiology of female breast cancer. Pollán M. Method 77 (2013) 71-75.

La entrada Breast cancer and its prevention se publicó primero en Neolife.