With all the IFing (predominantly male led as well) devotees, I have been perplexed by my inability to pull it off as a lady. Obesity Definition Obesity is an abnormal accumulation of body fat, usually 20% or more over an individual's ideal body weight. Obesity is associated with increased. If you want to count fat grams, look on food labels for the total fat in grams. Ignore the percent and the fat calories. One size doesn't fit all when it comes to fat.
Dietary Estrogens & Male Fertility. In my video, The Role of Diet in Declining Sperm Counts, I discussed the association between high saturated fat intake and reduced semen quality. One of the most recent papers on the topic found that a significant percentage of the saturated fat intake in the study was derived from dairy products. Residues of industrial chemicals may bioaccumulate up the food chain into animal fat, and some of these lipophilic (fat- loving) chemicals may have hormone- disrupting abilities. The U. S. Environmental Protection Agency performed a national survey of persistent, bioaccumulative, and toxic pollutants in the U.
S. The EPA team noted that since milk fat is likely to be among the highest dietary sources of exposure to these pollutants, it. The team tested milk from all over the country and found a veritable witches brew of chemicals. They estimate that dairy products alone contribute about 3.
Xenoestrogens like polychlorinated biphenyls (PCBs) are associated with the fats of fish or animal flesh and cannot be fully removed by washing and cooking, and so can accumulate in our fat, too. Xenoestrogens are chemicals with demasculinizing or feminizing effects. But even in a non- polluted world, animal foods also have actual estrogens, which are unavoidable constituents of animal products. All foodstuff of animal origin contains estradiol, which is at least 1. By drinking a glass of milk, a child’s intake of estradiol is 4,0.
Modern genetically- improved dairy cows can lactate throughout their pregnancy. The problem is that during pregnancy, estrogen levels can jump as much as 3. Cheese intake has specifically been associated with lower sperm concentration, whereas dairy food intake in general has been associated with abnormal sperm shape and movement.
Lower sperm concentrations by themselves may just represent a potential suppression of sperm production due to higher estrogen levels, but abnormal shape and movement suggests that dairy intake may be implicated in actual direct testicular damage. While milk products supply most of our ingested female sex steroids, eggs are a considerable source as well, contributing about as much as meat and fish.
This could be expected, as eggs are produced directly in the hens. In the U. S., anabolic sex steroids may be administered to animals for growth promotion, a practice banned in Europe twenty- five years ago. A study in New York found progressively lower sperm counts associated with processed meat consumption. However, similar studies in Europe after the ban found the same thing; so, it may not be the implanted hormones, but rather a consequence of other meat components, such as the saturated fat raising cholesterol levels. We. Twenty- five years later, we.
In the largest study to date, higher blood cholesterol levels were associated with a significantly lower percentage of normal sperm. Cholesterol was also associated with reductions in semen volume and live sperm count. These results highlight the role of fats in the blood in male fertility, and should be of concern given the rising prevalence of obesity and cholesterol problems. Although a healthier diet may be associated with healthier sperm counts, cholesterol- lowering statin drugs do not seem to help. What about the phytoestrogens in soy?
See The Effect of Soy on Precocious Puberty. More on hormones in dairy in: Neurotoxic chemicals in the dairy supply have been blamed for neurological conditions as well. See my video Preventing Parkinson.
In my video, The Role of Diet in Declining Sperm Counts, I discussed the association between high saturated fat intake and reduced semen quality. How long after drinking the lemon water should you wait to eat or drink anything else? Fertility Diet Q&A. How long does it take for the fertility diet to have its effect? There is a constant cycle of cells renewing themselves in the body.
Anabolic steroid - Wikipedia. This article is about androgens as medications. For androgens as natural hormones, see Androgen. Anabolic steroids, also known more properly as anabolic- androgenic steroids (AAS). They are anabolic and increase protein within cells, especially in skeletal muscles.
Conception problems becoming more and more common among today's couples. Read on to find out ways to boost male fertility and increase sperm count naturally, and to. Read visitors' weight control success stories using Ask the Dietitian® calculators. Read frequently asked questions about the Healthy Body Calculator®.
AAS also have varying degrees of androgenic and virilizing effects, including induction of the development and maintenance of masculinesecondary sexual characteristics such as the growth of the vocal cords and body hair. The word anabolic, referring to anabolism, comes from the Greek . The American College of Sports Medicine acknowledges that AAS, in the presence of adequate diet, can contribute to increases in body weight, often as lean mass increases and that the gains in muscular strength achieved through high- intensity exercise and proper diet can be additionally increased by the use of AAS in some individuals.
Their use is referred to as doping and banned by most major sporting bodies. For many years, AAS have been by far the most detected doping substances in IOC- accredited laboratories. Testosterone is now nearly the only androgen used for this purpose and has been shown to increase height, weight, and fat- free mass in boys with delayed puberty. These sports include bodybuilding, weightlifting, shot put and other track and field, cycling, baseball, wrestling, mixed martial arts, boxing, football, and cricket. Such use is prohibited by the rules of the governing bodies of most sports.
AAS use occurs among adolescents, especially by those participating in competitive sports. It has been suggested that the prevalence of use among high- school students in the U. S. Oral administration is the most convenient. Testosterone administered by mouth is rapidly absorbed, but it is largely converted to inactive metabolites, and only about 1/6 is available in active form. In order to be sufficiently active when given by mouth, testosterone derivatives are alkylated at the 1. This modification reduces the liver's ability to break down these compounds before they reach the systemic circulation.
Testosterone can be administered parenterally, but it has more irregular prolonged absorption time and greater activity in muscle in enanthate, undecanoate, or cypionateester form. These derivatives are hydrolyzed to release free testosterone at the site of injection; absorption rate (and thus injection schedule) varies among different esters, but medical injections are normally done anywhere between semi- weekly to once every 1.
A more frequent schedule may be desirable in order to maintain a more constant level of hormone in the system. In addition, because estered testosterone is dissolved in oil, intravenous injection has the potential to cause a dangerous embolism (clot) in the bloodstream. Transdermal patches (adhesive patches placed on the skin) may also be used to deliver a steady dose through the skin and into the bloodstream. Testosterone- containing creams and gels that are applied daily to the skin are also available, but absorption is inefficient (roughly 1. Individuals who are especially physically active and/or bathe often may not be good candidates, since the medication can be washed off and may take up to six hours to be fully absorbed. There is also the risk that an intimate partner or child may come in contact with the application site and inadvertently dose himself or herself; children and women are highly sensitive to testosterone and can suffer unintended masculinization and health effects, even from small doses.
Injection is the most common method used by individuals administering AAS for non- medical purposes. Studies indicate that the anabolic properties of AAS are relatively similar despite the differences in pharmacokinetic principles such as first- pass metabolism. However, the orally available forms of AAS may cause liver damage in high doses. AAS were ranked 1. Long- term steroid abusers may develop symptoms of dependence and withdrawal on discontinuation of AAS. Recreational AAS use appears to be associated with a range of potentially prolonged psychiatric effects, including dependence syndromes, mood disorders, and progression to other forms of substance abuse, but the prevalence and severity of these various effects remains poorly understood. As a result, AAS users may get misdiagnosed by a psychiatrist not told about their habit.
Case reports describe both hypomania and mania, along with irritability, elation, recklessness, racing thoughts and feelings of power and invincibility that did not meet the criteria for mania/hypomania. Compared with individuals that did not use steroids, young adult males that used AAS reported greater involvement in violent behaviors even after controlling for the effects of key demographic variables, previous violent behavior, and polydrug use. The drug response was highly variable.
However: 8. 4% of subjects exhibited minimal psychiatric effects, 1. The mechanism of these variable reactions could not be explained by demographic, psychological, laboratory, or physiological measures. There have been anecdotal reports of depression and suicide in teenage steroid users. A 1. 99. 2 review found that AAS may both relieve and cause depression, and that cessation or diminished use of AAS may also result in depression, but called for additional studies due to disparate data. Most of these side- effects are dose- dependent, the most common being elevated blood pressure, especially in those with pre- existing hypertension. For example, AAS may prematurely stop the lengthening of bones (premature epiphyseal fusion through increased levels of estrogen metabolites), resulting in stunted growth. Other effects include, but are not limited to, accelerated bone maturation, increased frequency and duration of erections, and premature sexual development.
AAS use in adolescence is also correlated with poorer attitudes related to health. Development of breast tissue in males, a condition called gynecomastia (which is usually caused by high levels of circulating estradiol), may arise because of increased conversion of testosterone to estradiol by the enzyme aromatase. This side- effect is temporary; the size of the testicles usually returns to normal within a few weeks of discontinuing AAS use as normal production of sperm resumes. Alteration of fertility and ovarian cysts can also occur in females. The kidney damage in the bodybuilders has similarities to that seen in morbidly obese patients, but appears to be even more severe.
Water- soluble peptide hormones cannot penetrate the fatty cell membrane and only indirectly affect the nucleus of target cells through their interaction with the cell. However, as fat- soluble hormones, AAS are membrane- permeable and influence the nucleus of cells by direct action. The pharmacodynamic action of AAS begin when the exogenous hormone penetrates the membrane of the target cell and binds to an androgen receptor (AR) located in the cytoplasm of that cell. From there, the compound hormone- receptor diffuses into the nucleus, where it either alters the expression of genes. It has been hypothesized that this reduction in muscle breakdown may occur through AAS inhibiting the action of other steroid hormones called glucocorticoids that promote the breakdown of muscles. Through a number of mechanisms AAS stimulate the formation of muscle cells and hence cause an increase in the size of skeletal muscles, leading to increased strength. Depending on the length of use, the side effects of the steroid can be irreversible.
Processes affected include pubertal growth, sebaceous gland oil production, and sexuality (especially in fetal development). Some examples of virilizing effects are growth of the clitoris in females and the penis in male children (the adult penis size does not change due to steroids.
Men may develop an enlargement of breast tissue, known as gynecomastia, testicular atrophy, and a reduced sperm count. Compounds with a high ratio of androgenic to an anabolic effects are the drug of choice in androgen- replacement therapy (e. Determination of androgenic: anabolic ratio is typically performed in animal studies, which has led to the marketing of some compounds claimed to have anabolic activity with weak androgenic effects. This disassociation is less marked in humans, where all AAS have significant androgenic effects.
The VP weight is an indicator of the androgenic effect, while the LA weight is an indicator of the anabolic effect. Two or more batches of rats are castrated and given no treatment and respectively some AAS of interest. The LA/VP ratio for an AAS is calculated as the ratio of LA/VP weight gains produced by the treatment with that compound using castrated but untreated rats as baseline: (LAc,t.
The LA/VP weight gain ratio from rat experiments is not unitary for testosterone (typically 0. Animal studies also found that fat mass was reduced, but most studies in humans failed to elucidate significant fat mass decrements. The effects on lean body mass have been shown to be dose- dependent. Both muscle hypertrophy and the formation of new muscle fibers have been observed. The hydration of lean mass remains unaffected by AAS use, although small increments of blood volume cannot be ruled out. After drug withdrawal, the effects fade away slowly, but may persist for more than 6.
Overall, the exercise where the most significant improvements were observed is the bench press. AR agonists are antigonadotropic . By suppressing endogenous testosterone levels and effectively replacing AR signaling in the body with that of the exogenous AAS, the myotrophic- androgenic ratio would be expected to be further increased, and this hence may be yet an additional mechanism contributing to the differences in myotrophic- androgenic ratio. In addition, some AAS, such as nandrolone, are also potent progestogens, and activation of the progesterone receptor is antigonadotropic similarly to activation of the AR.
Shattering the Myth of Fasting for Women: A Review of Female- Specific Responses to Fasting in the Literature. One of the more esoteric but much beloved tools in the paleo dieter’s tool- kit is intermittent fasting. What is intermittent fasting? IF is the practice of maintaining overall caloric intake while consuming those calories in fewer meals or in reduced time windows throughout the day. The goal is to create conditions of fasting in the body, but not for extreme lengths of time. Some examples of intermittent fast strategies include 1. The evolutionary premise — the argument that proponents of intermittent fasting make — is that humans evolved to optimize their health under less- than- optimal conditions.
Fasting, they say, is a natural and perhaps even necessary part of being human. Amazingly enough, this happens without any of the psychological crippling side effects of cravings and food obsession that practictioners of.
It is wholly understandable that fasting is all the rage these days. Sort of. I have a specific interest in intermittent fasting because of what I have witnessed both in myself and in working with literally thousands of women in the Pf. W community. Many women report to me (read more about that in this awesome book) that intermittent fasting causes sleeplessness, anxiety, and irregular periods, among many other symptoms hormone imbalance, such as cystic acne. I have also personally experienced metabolic distress as a result of fasting, which is evidenced by my interest in hypocretin neurons.
Hypocretin neurons are one way in which intermittent fasting may dysregulate a woman’s normal hormonal function. After my own bad experience with IF, I decided to investigate intermittent fasting. I looked into both a) the fasting literature that paleo fasting advocates refer to, and b) the literature that exists out in the metabolic and reproductive research archives.
Intermittent fasting and women: problems in paleo. What I found is that the research articles cited by Mark’s Daily Apple. This startled me because the article MDA cited was for me one of the strongest proponents of sex- specific differences in response to fasting. Sex differences were relevant. Still, the mere fact of being more sensitive to fasting simply by being a woman is, I would assert, pretty important for a woman who is contemplating or already practicing IF.
This goes nearly unmentioned in the blogosphere. Intermittent fasting and women: problems in the literature. Beyond reporting biases in the blogosphere, there remains an even greater problem of a significant testing bias in the fasting literature. Searching “men” + “intermittent fasting” in a Harvard article database yields 7. Searching “women” yields 1.
The animal studies are more equitable, but also a bit less applicable to human studies. There is an infertility condition – called hypothalamic amenorrhea – that millions of women suffer from due to being overly restrictive. But what of fasting? Intermittent fasting and women: should women fast?
The few studies that exist point towards no. It is not definitive, since the literature is so sparse, and it necessarily differs for women who are overweight versus normal weight (and who have different genetic makeups), but when it comes to hormones, women of reproductive age may do well to err on the side of caution with fasting. What follows first is a brief review of what can be gleaned in sex- specific responses to fasting in animal studies. Afterwards I talk about what has been concluded by the few relevant human studies.——————————————————————- Mice and Rats. First up is a study that demonstrates the. Comparatively, the males’ genetic response was less specific, suggesting that the males respond to a general stressor but they seem to lack the ability to discriminate between a high energy and low energy stressor.”Moreover, “IF down- regulated many gene pathways in males including those involved in protein degradation and apoptosis, but up- regulated many gene pathways in females including those involved in cellular energy metabolism (glycolysis, gluconeogenesis, pentose phosphate pathway, electron transport and PGC1- .
Female reproductivity down- regulates. In the researchers’ own words: “our data show that at the level of gonadal gene responses, the male rats on the IF regime adapt to their environment in a manner that is expected to increase the probability of eventual fertilization of females that the males predict are likely to be sub- fertile due to their perception of a food deficient environment.”——————————————————- In the final relevant IF rat study I could find, researchers subjected rats to the same diets– to 2. Calorie- Restricted (CR) diets, as well as to alternate- day fasting diets, and monitored them over the long term for hormonal responses. To elucidate the physiological basis of sex differences in responses to energy intake, we maintained groups of male and female rats for 6 months on diets with usual, reduced . In response to 4. CR, females became emaciated, ceased cycling, underwent endocrine masculinization, exhibited a heightened stress response, increased their spontaneous activity, improved their learning and memory, and maintained elevated levels of circulating brain- derived neurotrophic factor. Additionally, there was no significant change in the cognitive ability of the males on the 4.
CR diet. Males and females exhibited similar responses of circulating lipids (cholesterols/triglycerides) and energy- regulating hormones (insulin, leptin, adiponectin, ghrelin) to energy restriction, with the changes being quantitatively greater in males. The high- fat/high- glucose diet had no significant effects on most variables measured but adversely affected the reproductive cycle in females. Heightened cognition and motor activity, combined with reproductive shutdown, in females may maximize the probability of their survival during periods of energy scarcity and may be an evolutionary basis for the vulnerability of women to anorexia nervosa. They also found this: The weight of the adrenal gland was similar in rats on all diets; however, when normalized to body weight CR and IF diets caused a relative increase in adrenal size, the magnitude of which was greater in females, compared with males. In contrast, both CR diets and the IF diet caused a decrease in the size of the ovaries. And this, bearing in mind that “daytime” for nocturnal rats is “nighttime” for humans: The daytime activity of females was doubled in response to IF, whereas the IF diet did not affect the activity level of males.
Nighttime activity levels of males and females were unaffected by dietary energy restriction. And this. Women experienced no significant change.
After 3 weeks of ADF, women but not men had an increase in the area under the glucose curve. This unfavorable effect on glucose tolerance in women, accompanied by an apparent lack of an effect on insulin sensitivity, suggests that short- term ADF may be more beneficial in men than in women in reducing type 2 diabetes risk. Feelings of fullness were significantly (P. That’s all that exists! Women don’t have much to go on. There are a few rodent studies. They found that when alternate- day fasting,female rats and found significant negative hormonal changes occurring in the females.
There are even fewer human studies. Human studies on alternate day fasting have not been conducted on women of reproductive age at all, nor have any studies analyzed reproductive responses to fasting.
Another important distinction to make is between different body weights. Overweight and obese patients appear to experience significant improvements with IF regimes, but normal weight patients do not show the same across- the- board benefits. For women this may be a particularly sensitive issue. Overweight women may experience metabolic benefits, whereas normal weight women do not. I suspect that that may roughly be the case, but who knows.
Honestly, no one at this point. The practical solution, then, I believe, is to look at options, to be honest about priorities, and to listen to one’s body with awareness and love. Is fasting worth trying if a woman is overweight and trying to improve her metabolic markers, and so far hasn’t had much success? But the literature is so sparse in this area that we cannot make any real statements or predictions about the effects of fasting, other than that we just don’t know, and that we should continue to.
There are boatloads of others. If you’re interested in reading about the collective set of them and learning how to optimize female skin, weight loss, and hormone balance, for a few examples, you could do worse than my best- selling! What do you think?- -- -- -- -So, just as a heads up - some links above may be my affiliate links, which means I get a small commission if you click on it and make a purchase. Doing so is no additional cost to you, but helps me tremendously. Your support is SO greatly appreciated, so thank you in advance if you choose to do so. Check out my entire disclosure to know exactly how things work.