I feel like I’ve been bombarded lately with questions about fad diets. They’ve always been around, but they just don’t seem to go away.
It just seems shiny and new to try a “new” diet instead of sticking to the fundamental principles of a healthy one.
I’ve been noticing this more and more, with the incredible popularity of “keto” which is pretty much paleo circa 2012, and with new books sent to me for my feedback like The Sirtfood Diet (Find it here).
I was able to read and review The Sirtfood Diet, a plan that claims to help you lose 7 pounds in 7 days, all with the power of what they call “Sirtfoods” which are essentially antioxidants, polyphenols, and other health supportive compounds.
What are the kinds of foods the Sirtfood diet wants you to eat? Things like buckwheat, soy, strawberries, turmeric, red onions, kale, dates, garlic, and olive oil, among others. Besides buckwheat (for some) and soy, I had a hard time figuring out how these foods were so lacking in typical healthy diets like the authors claim.
Most people who promote a paleo diet include ample amounts of these, and sometimes the dark chocolate and red wine pictured on the cover, as well-rounded parts of the diet.
Reservetrol, a healthful component the diet authors claim is often missing is available in fabulous multi-vitamin supplements like this one and in many foods like blueberries and cranberries, besides red wine.
Polyphenols are also common across the range of plant based foods and are even available as powders to mix with smoothies (like this one). Most paleo authors value and promote the inclusion of lots of plant based foods in the diet.
Here’s the truth as I see it. The reason you might lose 7 pounds in 7 days is because the first three days consist of 1000 calories of mostly green juice. This is a common trend among fad diet plans- starve you during the first week while you’re motivated (while also telling you that you aren’t starving but are instead “detoxing” which is why you feel like you’re starving) and then working calories up to more maintainable levels so you continue to lose weight but think you are eating much more.
You’re losing water that first week. A little fat is lost too, but its almost scientifically impossible to lose 7 pounds of pure body fat in one week for the average person. It requires a caloric deficit that not even 1000 calories a day can meet.
I have no issues with a diet that supports the inclusion of healthy ancient foods. My mind has changed over the years with regard to gluten-free grains and other dietary components, so long as they are healthy FOR YOU.
The key to lifelong weight loss is learning how to heed your internal cues. Learning your body, understanding its needs, and feeding it nutrient dense food. There doesn’t need to be a special superfood protocol. There just needs to be balance.
I’m never going to say its ok to eat mostly bacon and butter. They’re nice as inclusions, but they don’t have the nutrient density that vegetables do.
I’m never going to be cool with women fasting. Thankfully the Sirtfood diet and I agree on that one (though I still think 1000 calories a day for a woman is pushing it, even for 3 days). If the choice is between you eating or not eating, I’m always going to say, eat.
But eat what makes your body feel good. I know what that looks like for most people- vegetables, fruit, meat, fat. Eat those things, in balance with the other things. with a focus on quality. That’s all you really need. And that’s what Weight Loss Unlocked is all about.
If weight loss has become a struggle following that paradigm, then you should look into seeing a professional. A good functional nutritionist in your area can help you get to the bottom of what is going on and provide a structured plan that will help you reach your goals, along with the accountability and monitoring to help you truly maintain that weight loss.
Please, oh please, don’t just go looking for another crash diet. In the end, you’ll lose much more than some money and a few pounds.
One of the most common problems I encounter in my audience is binge eating. This is also one of the most common concerns Noelle and I field for our podcast. Everybody wants to know: How do I stop?
I have written about overcoming binge eating at great length before. In the article Binge/Restrict: The Most Common Pattern of Overeating and How to Stop, for example, I argue that while most people think the solution to binge eating is simply to be disciplined enough to get over it, the answer is actually the opposite. The answer, I argue, is to allow yourself abundance. The answer, I argue, is lots of food. Once you stop restricting your diet, you no longer feel the deprivation and obsession that inevitably cause you to overeat later on.
I do still believe that this is one of the most important things you can do to overcome binge eating. But I would like to discuss here the great, biochemical heft behind these processes.
Because here’s the thing: as much as society (and you!) may call you undisciplined, stupid, lazy, gluttonous, fat, insert demoralizing adjective here, for bingeing on whatever kind of food has hooked you, it’s wrong. It’s just plain wrong. You’re up against a huge set of biological, habituated compulsions. Bingeing behavior has now been proven to have potent biological motivators. And you must know it. I believe — I hope — that as you know it, so you may forgive yourself. Then you may more easily walk the path of healing.
To that end, I am going to describe two separate studies. These were both done on rats, so of course we cannot assume they to apply to humans. But there are human analogues and other human studies (such as on the science of sugar addiction – a topic for another time), that indicate the models may well apply.
This study investigates the difference between constant, non-restricted access to palatable foods versus restricted access to palatable foods. It ends up revealing that just a few weeks of occasionally being exposed to bursts of sweetened milk cause rats to binge on it, as well as to maintain these eating habits even after the time restrictions have been taken away. It happens because of neural changes that have taken place during the “burst” period. These changes cause long-term habits to form.
Teri Furlong and colleagues at the University of Sydney gave rats a diet of either normal chow or chow plus sweetened condensed milk. The “normal chow” rats were the control group. The rats that received the sweetened milk were divided into two groups: half got milk all day every day, as much as they wanted. The other half got access to the sweet stuff for only two hours every day.
After five weeks, the scientists trained all of the rats to press levers. There were two levers: one for sweet sugar pellets and one for simple grain pellets. In the test, the animals feasted on one of the types of food (either the sugar or the grain) and then exposed to a lever. In the first scenario, rats saw the lever for food they hadn’t yet had. If they had eaten sugar, they got grain. If they had eaten grain, they got sugar. In this scenario, all the rats ate a lot of the new food. Tastebuds like variety.
In the second scenario, the rats were given access to levers for the food they had already eaten. So if they had eaten sugar, they got a lever for sugar, and if they had eaten grain, they got a lever for grain. And this is where things really get interesting: rats who had had constant access to the sweetened milk in the training phase ate to satiety. They stopped pressing the lever. They had no interest in either the grain or the sugar. But, rats who were only allowed access to the sweet milk for two hours a day (and for the rest of the day, as much unsweetened food as they wanted), responded differently. They kept pressing for grain, even though they were already full of grain, and they kept pressing for sugar, even though they were already full of sugar. They weren’t pushing these levers because they were hungry. They were pushing these levers because having restricted bouts of access to sweet foods rewired their brains.
Interestingly enough, the researchers found that the obsessive lever-pressing was associated with an area of the brain called the dorsolateral striatum–an area of the brain associated with habitual behaviors. The researchers therefore hypothesize that rats develop long-lasting bingeing behaviors because of the repetitive training they had from the easier phase of the study. In that phase, they simply learned that the sweet stuff was rarely available, so they stuffed their faces when they could. This imprinted in them a long term habit.
Importantly, chemicals injected into their brains that interfered with glutamate and dopamine activity in the dorsolateral striatum caused the bingeing behavior to stop.
In this study, MM Hagan and DE Moss subjected rats to four different patterns of 12-week restriction-refeeding cycles. The animals were either food restricted–constantly on a diet–or restricted plus some free-access binge days. After 12 weeks all rats underwent a re-feed period.
There were four different groups of rats: 1) “normal diet” eating with normal chow in the refeed period, 2) cyclical restricted eating (bingeing) with normal chow in the refeed period, 3) “normal diet” eating with palatable food in the refeed period, and 4) cyclical restricted eating (bingeing) with palatable food in the refeed period.
The rats that ate the “diet eating” consistently received 75% of their normal calorie intake. The rats with cyclical restricted eating went through 4 days of restriction of 75% of their normal intake, then two days of a refeed where they could eat ad libitum.
After 12 weeks of this kind of entrainment, the rats were given 3 tests: 1) 24 hour deprivation and chow feeding; 2) 24 hour deprivation then chow and cookie feeding; 3) spontaneous chow and cookie feeding.
In the first test, with 24 hour deprivation and chow feeding, the rats which had gone through restricted cycles of feeding (on both normal and sweet food) ate 10% more food than the control rats. Interestingly enough, the rats that had been conditioned on sweet food were not all that interested in the chow feeding, and actually ate 20% less chow than the control group.
In the second test, with 24 hour deprivation and cookie feeding, rats that had been in sweet restricted cycles ate almost 20% more food than the control group.
In the third test, in simple spontaneous feeding without a 24 hour deprivation window, rats conditioned by sweet foods ate more than rats on normal chow, regardless of whether they had been restricted or not. The rats who ate non palatable chow and were on normal “diets” were perfectly fine; the rats who had eaten sweets but were on a normal diet ate about 20% more; the rats who had been in restricted cycling patterns and refed on sweets ate 80% more than control mice on normal diets. 80% more.
Researchers in this study conclude, therefore, that “of all the conditions, the restricted/palatable group showed the most bulimic-like eating behavior. That is, a history of restricted eating (dieting) and refeeding on palatable food (bingeing) predicted a persistence of bingeing-eating behavior even after a 30-day period of normalization.”
Other Studies and implications
Of course, these are just two studies, and have been conducted on rats. There are plenty of indicators that similar phenomena are at play in human beings. Recall perhaps most strikingly of all the Minnesota semi-starvation experiment in which “normal men” were food restricted and showed binge eating and insatiable appetites for sweet foods even after many days of unrestricted eating during the rehabilitation phase (Franklin et al 1948). In the 90s, Polivy et al “found that uncontrollable bouts of binge eating were significantly more common among prisoners of WWII who had, over 50 years earlier, experienced severe food restriction compared with nonrestricted combat veterans” (1994).
Via experiments on rats, we can see more clearly mechanisms by which this takes place. Apparently, pleasure neurotransmitters (such as dopamine) are definitely involved, as are, to a significant extent, the parts of the brain that are associated with habit formation.
The bottom line is this: your history of dieting, of binge eating, of restricting and refeeding, has had a concrete affect on the functioning of your brain. I can’t tell you how many thousands of women have expressed terrible guilt and shame with respect to their bingeing behaviors. They are all incorrect. If you feel this way, you are also incorrect. Your biology compels you, and powerfully so.
As I indicated in the start of this post, literally the best thing you can do for yourself is to forgive yourself. Give yourself access to food, and unlimited. Accept your body and delight in how hard it tries for you. Provide it with the nourishment it needs to develop new habits.It may feel rough at first, but over time the body can actually learn to eat well. You may also find that staying away from sweets or certain palatable foods is important. So long as this does not cause you to develop obsessions with these foods, that could be good. It would remove the biological trigger of habit that you have imprinted in your brain. Even switching to a different set of palatable foods could help (so long as your access is unrestricted). They key here is developing a positive, loving, forgiving attitude and helping your body create new habits.
You may also wish to supplement with low doses of l-tyrosine and/or l-tryptophan. These are precursors to dopamine and serotonin, respectively. They have been demonstrated to sometimes be quite potent for curbing people’s compulsions to overeat (an argument famously made by Julia Ross in The Diet Cure). I have personally noticed that when I take L-tryptophan (I take it for sleep) my constant feeling of “I could eat” disappears, and I feel more like a “normal person.”
Do you have experience that lines up with what I’ve discussed here? Contradicts it? I’d love to hear about what you’ve gone through, and anything you share could be a great help to someone else in the community.
One of the more esoteric but much beloved tools in the paleo dieter’s tool-kit is intermittent fasting.
What is intermittent fasting? I.F. 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 10, 8, or 5 hour eating windows throughout the day, or perhaps eating just two meals each day: one in the morning, and one at night. The evolutionary premise — the argument that proponents of intermittent fasting make — is that humans evolved to optimize their health under less-than-optimal conditions. Intermittent fasting, they say, is a natural and perhaps even necessary part of being human.
The modern-day scientific correlate appears promising, too:
Most people are nowadays aware that a calorie-restricted diet has the ability not just to decrease body weight but also to lengthen a human life. Emerging research is beginning to show, however, that intermittent fasting is just as effective as calorie restriction in ensuring these health benefits! Amazingly enough, this happens without any of the psychological crippling side effects of cravings and food obsession that practictioners of calorie-restriction often experience.
Intermittent fasting women is a specific interest of mine because of what I have witnessed both in myself and in working with literally thousands of women in the PfW 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 have the ability to incite energetic wakefulness, and to prevent a person from falling asleep, in reaction to the body detecting a “starved” state. 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 Women: Problems in the Paleosphere
What I found is that the research articles cited by Mark’s Daily Apple (and others), focus on health benefits such as cancer-fighting properties, insulin sensitivity, and immune function.
However. I was struck by what seemed like an egregious sex-based oversight in that MDA post I linked to above. MDA cites this article as a “great overview” of the health benefits of intermittent fasting. 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 in two striking areas:
1) women in studies covered by the review did not experience increased insulin sensitivity with IF regimes and
2) intermittent fasting women actually experienced a decrease in glucose tolerance.
These two phenomena mean that women’s metabolisms suffered from IF. The men’s metabolisms on the other hand improved with IF across the board. Recall that the review was reported by MDA as “a great overview of benefits [of IF].”
Secondly, in another fasting post at MDA, of which there are many, the health benefits of fasting are listed and reviewed, but the sex-specific aspects of the hormonal response go unmentioned, and reproduction/fertility/menstrual health isn’t mentioned at all.
This is not to say that Mark is not attentive to who should and who should not be fasting. He knows very well and cautions people against the dangers of fasting while stressed. 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 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 71 peer-reviewed articles. Searching “intermittent fasting women” yields 13, none of which are a) solely about women b) controlled studies or c) about more than body weight or cardiovascular benefits.
The animal studies are more equitable, but also a bit less applicable to human studies.
It is well-known in both the research and the nutritional communities that caloric restriction is horrible for female reproductive health. This is not news. 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 Women: Should we 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 & Rats
First up is a study that demonstrates the hippocampal changes of calorie restriction and intermittent fasting for both male and female rats. In this study, they do alternate day fasting, which entails free eating on one day and a fast day on the next.
The study found that brain states while fasting were different for male and female rats. For male rats the change in hippocampus size, hippocampal gene expression, and ambulatory behavior was the same no matter what kind of restricted diet they were on – but for female rats, the degree of change in brain chemistry and in behavior was directly proportional to degree of calorie intake, demonstrating the unique sensitivity of female rats to the starvation response.
” The organization of the females’ response to the energy restricted diets is suggestive of some underlying mechanism that may allow for an organized, pre-programmed, response to enhance survival in times of food scarcity. 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-α), cell cycle regulation and protein deacetylation.” In this study, both male and female rats gained small amounts of weight on IF diets.
For female rats, even in the most innocuous form of restriction–intermittent fasting–significant physiological changes take place. Male rats do not experience as dramatic hippocampal and general brain chemistry change as female rats do, and their behaviors, specifically their cognition and their dirunal and nocturnal activity, do not change.
Female rats, on the other hand, “masculinize.” They stop ovulating and menstruating. They become hyper-alert, have better memories, and are more energetic during the periods in which they are supposed to be sleep. Theoretically, according to these researchers, this is an adaptive response to starvation. The more the female rats need calories– or at least the more their bodies detect a “starvation” state– the more they develop traits that will help them find food. They get smart, they get energetic, they get active, and they stop sleeping.
In a follow-up study conducted by the same researchers who explored the masculinzation of female rats, the researchers analyzed the gonadal transcription of male and female rats subjected to IF regimes.
This study found that male reproductivity up-regulates in response to metabolic stress. Female reproductivity down-regulates.
Completely opposite to the female rats becoming infertile while fasting, male rats become more fertile. 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 20 and 40 percent Calorie-Restricted (CR) diets, as well as to alternate-day fasting diets, and monitored them over the long term for hormonal responses. The results were striking. Below is the abstract in full because it’s so powerful:
Females and males typically play different roles in survival of the species and would be expected to respond differently to food scarcity or excess. 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 [20% and 40% caloric restriction (CR), and intermittent fasting (IF)], or elevated (high-fat/high-glucose) energy levels and measured multiple physiological variables related to reproduction, energy metabolism, and behavior.
In response to 40% 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. In contrast, males on 40% CR maintained a higher body weight than the 40% CR females and did not change their activity levels as significantly as the 40% CR females. Additionally, there was no significant change in the cognitive ability of the males on the 40% 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.
The testicular weight was unaffected by any of the diets. 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.
Uterine activity was monitored daily with vaginal smear tests; cyclicity was scored as regular, irregular, or absent. The mild energy-restriction diets (20% CR and IF) significantly increased the proportion of animals displaying irregular cycling patterns, whereas the 40% CR animals displayed an almost complete loss of estrous cyclicity.
In males, corticosterone levels were elevated only in response to the 40% CR diet, whereas in females corticosterone levels were significantly elevated in response to all three energy-restriction diets, suggesting a relative hyperactivation in females of the adrenal stress response to reduced energy availability.
For lipids, all the rats did well: “Collectively, these data suggest that atherogenic profiles of both males and females are improved by dietary energy restriction.” Interestingly, too, as they pointed out in the abstract, human females also perform cognitively much “better” (memory and alertness) on CR and IF diets than on normal feeding schedules.
There are of course some caveats to this study: A) They are rats. B) They are somewhat “metabolically morbid” rats, which may make them more susceptible to disease. C) The rats were allowed to eat ad libitum on the IF days, but they simply did not meet their caloric requirements this way. So while it is a somewhat natural form of IF, it is still calorically reduced, such that that must be taken into account when gasping in horror at the hormonal responses of IF-ing female rats.
The Few Human Studies
I mentioned above that through the same review that MDA used as a “great overview” of IF benefits for all sexes, I found harmful metabolic effects for women subjected to alternate-day fasting regimes.
This is the study:
Heilbronn et al found that with IF, insulin sensitivity improved in men (21 participants) but not in women (20 participants): after three weeks of alternate day fasting, insulin response to a test meal was reduced in men. Women experienced no significant change. “It is interesting that this effect on insulin sensitivity occurred only in male subjects,” they report.
With respect to other health markers female health actually declined, specifically with respect to glucose tolerance:
“Another diabetes risk factor that has shown a sex-specific effect is glucose tolerance. 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. ” The opening line of their discussion reads: “Alternate day fasting may adversely affect glucose tolerance in nonobese women but not in nonobese men.”
In a follow up study, Heibron et. al studied the effects of alternate-day fasting on cardiovascular risk. When human subjects fasted on alternate days for another three week period, circulating concentrations of HDL cholesterol increased, whereas triacylglycerol concentrations decreased. This is a good thing. However, the shifts in lipid concentrations were shown to be sex specific: ie, only the women had an increase in HDL-cholesterol concentrations, and only the men had a decrease in triacylglycerol concentrations.
This study of alternate day fasting included 12 women and 4 men. In eight weeks, body weight decreased by about 10 pounds, and body fat percentage decreased from 45 to 42. Blood pressure decreased, total cholesterol, LDL cholesterol, and traicylglycerol decreased. These people were significantly obese, which limits the results of this study to an obese population. However, “perimenopausal women were excluded from the study, and postmenopausal women (absence of menses for >2 y) were required to maintain their current hormone replacement therapy regimen for the duration of the study.” (Their words, my emphasis)
The one, big study of intermittent fasting conducted on men and women looked at differences between isocaloric feeding schedules: 3 meals/day feeding versus 1 meal/day.
The study focused on body weight composition, blood pressure, and body temperature in subjects. Subjects were fed isocalorically either one meal each day or three meals each day. All subjects were between 40 and 50 years old (excluding women of reproductive age), and between BMIs of 18 and 25. They ate, so far as I can tell, a healthy diet with 35 percent fat, PUFA < MUFA < SFA. Only 15 of the original 69 completed the study (which goes to show just how fun everyone thought fasting was). As for the results,
“Systolic and diastolic blood pressures were significantly lowered by ≈6% during the period when subjects were consuming 3 meals/d than when they were consuming 1 meal/d. No significant differences in heart rate and body temperature were observed between the 2 diet regimens. Hunger was enormously larger in the one meal/day than in the three meals/day group. “The 1 meal/d diet was significantly higher for hunger (P = 0.003), desire to eat (P = 0.004), and prospective consumption (P = 0.006) than was the 3 meals/d diet. Feelings of fullness were significantly (P = 0.001) lower in the 1 meal/d than in the 3 meals/diet.” Body weight dropped only four pounds after several months. Cortisol dropped, but Total, LDL, and HDL cholesterol were 11.7%, 16.8%, and 8.4% higher, respectively, in subjects consuming 1 meal/d than in those consuming 3 meals/d.
In sum: patients on the one meal/day regiment were unhappy, hungry, lost a little bit of weight, increased cholesterol. This was a small sample, included somewhat menopausal women, and all people of normal body weight.
Intermittent Fasting Women: In Conclusion
All that being said, that’s it. 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.
Moreover, the few studies that have been conducted on non-obese women have demonstrated that their metabolic responses are not nearly as robust as those of men, and may in fact be antagonistic to their health.
This post has focused on sex-specific responses to fasting, specifically intermittent fasting women. 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? Perhaps. Should it be undertaken if a woman is of normal weight? What if she is a light sleeper? What if her periods begin to dysregulate? Or stop? What if she starts getting acne, getting a stronger appetite, or losing her appetite altogether? These things happen, and I see them in women who fast and contact me time and time again.
We women (people!) should be honest with ourselves about our priorities, and act constantly with our mental and physical health foremost in our minds. All women are different. 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 emphasize the centrality of awareness, caution, and loving nourishment in moving forward.
IF is one realm in which the female body has unique characteristics and needs that demand attention. 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 book, Sexy by Nature,here.
This morning one of my most dear friends posted to Facebook that she was so happy after an interview she just conducted with Mark Sisson.
The reason she was so happy, at least in part, was that Mark helped her understand better how to re-fuel after a work out. Most fitness gurus know that muscle building is the most efficient when you refuel with carbohydrate and protein. This is a precise science that people talk about all the time.
What we forget to often talk about are the hormonal effects that occur at this time, too.
This is especially important for women.
When I was diagnosed with PCOS, I searched high and low for a link between muscles and testosterone. I thought maybe my high muscle mass was causing my PCOS. Exercise junkies on internet forums often hypothesized that this was the case…. that increased muscle mass causes women’s testosterone levels to go up. That made intuitive sense to these people. Men have muscles, and lots of testosterone.
But I couldn’t find any good science to back it up.
Today, still, women with high testosterone levels ask me all the time if their exercise habits have anything to do with it. Just last week I had to shrug my shoulders as a fellow blogger and say ‘hm sorry I don’t have a good answer for you?’
(By the way, I did write a book on PCOS, its causes, and how to support your body with it. See it here.)
Then Stacy and Mark gave me the idea to look into the science of post-workout meals.
Because what’s important for the relationship between exercise and testosterone levels is not muscle mass, nor even the intensity of the workout.
It is, instead, whether or not you eat afterwards.
What happens when you workout and afterward
During the course of any kind of strenuous activity — whether more in the vein of endurance / cardio or in high intensity weight lifting — the body burns through its glycogen stores. Glycogen, in essence, is a form of sugar. It’s stored in the muscles. It’s one of the body’s favorite fuel sources for exercise. Athletes almost always start a demanding workout with full glycogen stores. Otherwise, they will have less fuel for their efforts and will perform less than optimally.
Fitness specialists recomment that after a workout that depletes muscle glycogen (so after about one hour of higher intensity), you eat a meal composed of 3:1 carbohydrate:protein. When you do so, insulin and growth hormone levels rise, and testosterone levels fall. This boosts muscle building while at the same time maintaining healthy hormone balance. Cortisol levels appear to stay the same after you eat. For women, luteneizing hormone levels also stay the same . This demonstrates that it is not hormone levels in general that fall when you eat post-workout, but testosterone levels specifically.
Testosterone is important for a lot of functions in the female body. Excess testosterone, however, is not. Excess testosterone causes infertility, poly cystic ovarian syndrome, acne, male pattern hair growth on the face and body, hair loss on the top of the head, and diminished libido.
Here are some summaries of papers I recenty read to demonstrate these effects:
Kramer, Volek et al 1998 compared the hormonal responses to consecutive days of resistance training with and without nutritional supplementation. Subjects drank either a carbohydrate‐protein supplement 2 hours before and immediately after their workout or a placebo. Blood was taken before and 0,15,30,45 and 60 minutes after the workout. Lactate, growth hormone, and testosterone were significantly elevated immediately postexercise in all subjects. Growth hormone and prolactin responses on day 1 were significantly higher for supplementing subjects, then leveled out. After exercise, testosterone declined below resting levels for supplementing subjects during all three days. Glucose and insulin remained stable for placebo subjects and were significantly elevated by 30 minutes during supplementation. Insulin‐like growth factor‐I was higher during supplementation on days 2 and 3, indicating long-term increases in IGF1.
Chandler, Byrne, et al 1994 examined the effect of carbohydrate and/or protein supplements on the hormonal state of the body after weight training exercise. Subjects consumed either a control (water), protein, carbohydrate, or carbohydrate‐protein drink immediately and 2 hours after a resistance training workout. Blood samples were drawn before and immediately after exercise and during 8 hours of recovery. Exercise induced elevations in lactate, glucose, testosterone, and growth hormone in all groups. Carbohydrate and carbohydrate-protein stimulating insulin levels. Carbohydrate‐protein led to an increase in growth hormone 6 hours post exercise which was greater than protein and control. Supplements had no effect on insulin‐like growth factor‐I but caused a significant decline in testosterone. Testosterone levels fell below resting levels 30 minutes postexercise during all supplement treatments compared to the control.
Many people deliberately fast after a workout in order to burn as much fat as possible.
While this is a reasonable approach for people who are significantly overweight or who do only this only occasionally, women who repeatedly fast after workouts can experience significant long-term testosterone elevations.
I used to be one of these women. My testosterone levels were through the roof…. but I was completely insulin sensitive. Conventional wisdom says that insulin is the primary means by which testosterone becomes elevated in the body (it directly stimulates testosterone production in the ovaries). Clearly, insulin wasn’t my problem.
I can’t say that my daily high intensity workouts and limited fueling were the only cause of my high testosterone levels. Most definitely they were not.
But it seems that they were a culprit. And I can honestly say that deliberately refueling after every workout (like with awesomeness that is Tanka bars!) and dance class, along with being sure to include plentiful carbohydrates in my diet, relax as much as possible, and gain a few body fat percentage points, has drastically improved my sex drive and the quality of my skin.
The healthiest athletes I know – and some incredibly beautiful female fitness competitors, to boot – always, always, always refuel after a workout.
My body building friend Julia Ladewski of Bella Forza fitness. Image credit: Eva Cowan Fitness.
Check out more awesome snacks like smoked salmon, protein bars, and powerhouse paleo granola here.
Even if you are on a low carbohydrate diet, I — and low-carbohydrate gurus, too — recommend consuming some carbohydrates after your workout. Make it at least 30 grams of carbohydrate — so about two apples, or a half cup of rice — and 10 grams of protein, so 1-2 eggs, or half a can of tuna. Fasting after a workout very occasionally is okay. And it varies by individual. Nonetheless science doesn’t lie – a fasted workout decreases muscle growth, increases soreness, and elevates testosterone levels in women.
And, of course, for more on how to fast, and how many carbs and fat grams and the like to eat…
you can learn all about that in my book on weight loss for women Weight Loss Unlocked. To get a jump start on it, you can dowload a free chapter of the book HERE, and sign up for updates on more free weight loss tips and info!
And if you happen to suffer from acne as a result of your workouts or hormone balance, you may be interested in my brand new, right now 50% off program for overcoming acne, Clear Skin Unlocked: The Ultimate Guide to Acne Freedom and Flawless Skin.
Clear Skin Unlocked was written specifically for women like you in mind. It’s for when you’re frustrated, looking for answers, and tired of falling through the cracks. In Clear Skin Unlocked I discuss everything I did in this blogpost here at much greater depth, as well as provide a Four Week Jumpstart to Acne Freedomto get you on your way to robustly healthy and radiant skin, for good.
The following post is written by a lovely and powerful new voice in the body love scene. Her name is Madelyn, and she used to be a body builder.
I first came across Madelyn’s work I believe at some point in 2013. To be honest, I wasn’t a fan. I was perhaps even appalled. A bit horrified, maybe. Sad. Angry. I mean – it was okay. But what she was selling on her website, more or less, was herself as a muscle-glorified sex object.
Honestly, that’s got to be a hell of a body to let go of. I can’t even imagine what it’s like to step ‘down’ from so high a pedestal.
Now this is the kind of photo I used to look at and weep tears of envy.
If you go to her site today, you’ll see a lot of the same photos. These kinds of photos sell appearances more than health, which isn’t my favorite way to inspire people.
Yet with a keen eye, you’ll see, too, a woman on a hell of a journey of change, and a set of photos that tell a story.
Because while so many of the photos are the same, the language is different. Madelyn talks about “health” and “inner strength” and “acceptance.” Those photos are old, and she and doesn’t compete any more. Her invitation to join her mailing list reads like this:
“Ready to love your body? Sign up for the FREE eCourse “Mind Body Satisfaction, Sacrifice-Free” and learn how to fall in love with yourself exactly how you are. “
but anyway. It’s so powerful to witness someone coming through these changes and rocking them out. Madelyn now loves her body because of the way it feelsfar more than the way it looks.
Madelyn is over body building. And in love.
She recorded a hell of a youtube video about her journey –
– and if you’ve got ten minutes it’s definitely worth the watch.
Here she is, in her own words. You can find more of Madelyn (and her kickass podcast, which I was just recorded for last night) @ MaddyMoon.com.
The following story generally rings true for many people, which is why I’m such an open book in regards to my food and body issues growing up. Nobody is alone in this battle and there is most definitely a solution just waiting to be discovered. I am so glad I can now share my discovery of that solution.
I started my food obsession, body shaming, and negative self-worth at a really young age. When I was about 15 years old I watched a television show that warned against the dangers of anorexia, bulimia and the likes. Even though it warned against the tragic habit, it was the first time I had really heard about eating disorders and it stuck in my head as something to try out later and see what happened.
I wouldn’t say that I suffered from one specific eating “disorder” but I’ve had disordered eating most of my life. My relationship with food always depended on my relationship with my weight. And my relationship with weight depended on how “in control” I was of everything else. It was a terrible cycle that I seemed to never get out of.
I started the cycle as a vegetarian, mostly for animal rights, but it eventually turned into a weight control practice. I then realized I wanted the body of a fitness model and physique competitor, so I switched over to the meat eating clan and began to eat like a bodybuilder AKA six meals a day, every three hours, no salt, no fruit, everything had to be weighed and measured and eaten out of Tupperware. Soon enough, getting my body fat pinched every weekend was a typical activity, as well as my hour-long cardio sessions in the morning paired with lifting sessions in the evening. Amidst this loveless, foodless, deprived life, I was starting to become addicted to seeing my body transform. As the body fat melted off, my self-esteem skyrocketed. As my butt got rounder, my smile got larger.
After hitting the stage for my first and even second fitness competition, I gained a little weight back and returned to my average size. In fact, I was much stronger, healthier, happier, and fuller (physically and emotionally) but less toned. Womp, womp. The psychological struggles continued. I loathed my lack of leanness, I hated my distorted body image and I still measured and weighed my food in attempt to create that perfect body again.
Soon enough I discovered paleo after receiving a book to review for my blog, and then again, when a friend told me how awesome the “diet” had been for him. I became really interested and really involved in the community, where I met many people who taught me to love myself no matter what. Though this is easier said than done, after extreme commitment, positive affirmation, journaling, getting a dog, and moving states (not necessarily because of my body image struggles but it certainly didn’t hurt), I finally found something deep inside of me that was dying to come out.
Not just physical strength but emotional strength. I developed the strength to challenge social norms and to decide for myself what I think “beautiful” really means. In the end, I decided beautiful means life. It means coffee in bed on a Sunday morning. It means an extra spoonful of peanut butter just because. It means going four wheeling or boating whenever I want, because I no longer have to worry about bringing Tupperware meals. Last but not least, it means being able to tell myself “it’s okay” to not work out when I don’t feel like it. It’s okay to put family and friends FIRST before the gym and bulk cooking. It’s okay. Why? Because I’m already beautiful.
As many people say, paleo is not just a diet. It’s a lifestyle. It means to live organically, stress-free, happy and healthy. Healthy can be subjective but for most people, it means to live a life that promotes your version of optimal health. It means to live in a way that promotes mind-body satisfaction, without the sacrifices.
When I first discovered paleo, I went the strictest route. I basically did a Whole30 but for four months. I became too rigid and decided that wasn’t the healthiest for me, personally. I even discovered I have no allergies to gluten, dairy, beans or grains. While that’s kind of cool, I didn’t go crazy on eating them because as I listened to my body, I discovered those foods don’t necessarily make me feel optimal energy.
Truthfully, I rarely eat gluten or legumes by choice because they don’t make me the best version of myself. Dairy on the other hand makes me feel like a rock star.
So I make it work for me. Paleo has allowed me to find the best version of myself by helping me realize what makes me feel best, inside and out.
There are no meal plans, no food scales, no body fat pinchers, no tiny swimsuits hanging on my “inspiration wall” and certainly no sports-bra and spandex clad photo shoots in my near future.
I’m so excited to now have the “Madelyn Moon Diet” and nothing else. And more than just the diet aspect, I now live a much more minimalistic life. I try to keep my household minimalistic, as well as my face (less is more, ladies) and even my workouts!
The people I have met in the paleo community have literally changed my life in every aspect. I could name you ten people right now that have impacted me in some way or another and have brought me to tears from their support and generosity.
I am in no way exactly where I want to be in terms of body image and my relationship with food, but I am much farther in my journey than where I started. I have come incredibly far in all actuality, and as long as I remember to keep up the self-love and acceptance, I will be in the best “shape” of my life (possibly literally, but that one is more metaphorically).
Because I wanted to share how I’ve learned to retrain my brain into loving my body just the way it is, as well as block out all of the lean body fitness fluff, I created an eCourse that guides readers step by step on how to do exactly that. My goal with the course is to give you small, easily implemented changes you can make every day that will eventually lead you into non-negotiable self-love and body acceptance.
Lastly, I wanted to further share my passion for the ever-so-important mind body relationship by creating a podcast, called Mind Body Musings. The podcast features various guests that are well-known in the fitness industry who share their stories, theories, research and knowledge with us so that we can all better understand our bodies and brains. The podcast can be found on iTunes here, or you can go to my website here for the direct download links.
I also provide a free audioguide 4 Pillars of Femininity for Perfections, here.
A big thank you to Stefani for letting me share my story with you today. Stay tuned for this story to be published in The Paleo Miracle 2 as well, along with many other inspirational mind body strengthening stories.
I hope you enjoy any newfound insight you learn from these two tools and further develop your own strength, beauty and self-love.
There is a hell of a dichotomy occurring in the Paleo blogosphere this month. 99 percent of the time I am pleased as Pooh stuck up a honey tree, nestled in my esoteric corner of paleo-feminist rage, but every once in a while I wish more people could hear what I have to say. Today is one of those days.
The split I am talking about is not all that nefarious. In most cases, it’s benign and can be ignored. But in general I would like to draw attention to it, because I think there’s a lot going on beneath the surface (and here, the depths are not just Nemo and Dory but are instead people’s lives), and that depth requires speaking to. Immediately.
Mark’s Daily Apple has recently done a beautiful series on the benefits of fasting. I loved it. I learned plenty, as I always do on MDA. The series was well-written and -organized, and in fact I ended up directing people who are unfamiliar with fasting to the site in hopes of swaying their opinions. (So let it be clear: I am not against fasting per se.) Yet Chris Kresser has also done an April “Best your Stress” challenge. Serendipitously enough, it concludes today. And it is exactly what it sounds like: an endeavor to spend 30 days taking practical steps to counteract stress. Chris’s idea was that people often spend 30 days trying to get their diets in line. But what about their stress, and their lives? I couldn’t agree more. This man is a gale of fresh, important ideas.
The reason I say these two Big Themes are at odds is because they are. Fasting is a stressor. Period. Mark Sisson would agree. All people who advocate fasting would agree. But all they ever do is put an asterisk at the end of their posts: *people who are stressed should probably not fast, they say. But why? Who is affected, and how? What can fasting and other forms of restriction do to our brains, and to our lives?
What I want to draw attention to today are little loci that sit on the border of the hypothalamus called Hypocretin Neurons. Hypocretin neurons (also called Orexins–and note that the word “orexin” means “appetite increasing”) were discovered just 14 years ago in 1998, but they have radically altered the landscape of eating neurobiology since then. No, they are not the sole molecules responsible for sleep and waking. Mice that have had these neurons removed still sleep and wake in roughly normal patterns. But they never feel alert, and they never suffer insomnia. And when the neurons are activated, the mice leap into action. Hypocretin neurons wake animals up. This much is certain.
The lack of Hypocretin Neuron signalling is the cause of narcolepsy, while elevated Hypocretin levels induce arousal, elevate food intake, and elevate adiposity. Hypocretin Neurons upregulate the production of molecules down several other pathways, too: these include noradrenergic, histaminergic, cholinergic, dopamine, and serotonergic.
The anatomy of Hypocretin Neurons is also coming into greater light. When are the neurons active? What signals do they receive, and what signals do they produce? Research is beginning to show that Hypocretin Neurons are excited by excitatory synaptic currents and asymmetric synapses with minimum inhibitory input. The fact of asymmetry is important. It means that Hypocretin Neurons are instead always acted upon by mostly uniform – excitatory – signals they receive. Hypocretin Neurons only ever up-regulate and relax. They do not down-regulate. Excitatory signals outnumber inhibitory signals 10:1.
One notable source of excitation is corticotrophin releasing hormone, which suggests that stress activates the activity of Hypocretin Neurons. GABA neurons also create a bridge between Neuropeptite Y, which is the molecule that arguably has the strongest appetite-stimulating effect on the brain, and Hypocretin Neurons (more on Neuropeptide Y later this week). From there, Hypocretin Neurons project to all regions of the brain, including the hypothalamus, cerebral cortex, brain stem, and spinal cord. It seems as though Hypocretin Neurons may act as a nexus of signal input for the appropriate synchronization of various autonomic, endocrine, and metabolic processes.
Food restriction further augments recruitment of excitatory inputs onto Hypocretin cells. This explains the relationship between insomnia and adiposity: because of the easy excitability of Hypocretin Neurons, any signal that triggers their activity, regardless of homeostatic needs, will elevate the need to feed in brain circuits such as the locus coeruleus and the melanocortin system while also promoting wakefulness through activation of noradrenaline-stimulating neurons. Anything that promotes the release of corticotrophin releasing hormone (CRH) such as reduced sleep will further trigger Hyocretin Neuron firing and Appetite. This is a vicious cycle. Hypocretin Neurons play the role both of trigger and of accelerator, taking states of wakefulness, insomnia, stress, and obesity into continual positive feedback loops.
So how does leptin factor in? Hypocretin Neurons express leptin receptors. Moreover, some recent complicated neurobiological work done on mice has shown that injecting them with leptin decreases the activity of their Hypocretin Neurons. What this means is that Hypocretin Neuron activity is stimulated in part by decreasing levels of leptin in the blood, and that increased leptin levels reduce the level of excitation running through Hypocretin Neurons. This is coupled by ghrelin activity, which is also detected by Hypocretin Neurons. Ghrelin, which originates in the gut and is known to stimulate appetite, also excites Hypocretin Neurons. What does feeding do, then, for Hypocretin Neuron excitation? Experiments on mice show that re-feeding restores normal Hypocretin activity, to an extent. Repeated abuse takes longer to recover from, but the simple presence of leptin in the blood normalizes the brains of mice.
Hooray! This is good for fasting, right? So long as one re-feeds appropriately, everything should be fine? Well, yes. In a healthfully functioning individual. But not in a) someone who is both stressed and leptin resistant, since increased leptin levels from the re-feed might not be powerful enough to offset other excitatory pathways b) someone who is currently emerging from yo-yo dieting or caloric restriction c) someone who is dealing with an over-stimulated appetite, d) someone experiencing stress, e) someone who has had a history of insomnia, f) someone who is underweight, since they have low leptin levels, g) anyone who has ever had an eating disorder, particularly bulimia or binge eating disorder or h) anyone with HPA axis or endocrine dysregulation, particularly women, including overt stress, hypogonadism, hypothalamic amenorrhea, hypercortisolism, or hypocortisolism (adrenal fatigue.) I am sure the list is incomplete.
In animals, Hypocretin Neurons serve an important evolutionary function. Arousal is a vital behavior in all species. And normally, Hypocretin Neurons respond quickly to changes in input. But in situations of chronic metabolic or endocrine stress, or of recovering from a stressor, they can lead to hyper-activity and hyper-feeding.
Researchers have long known about the link between leptin, sleep, and obesity. The less someone sleeps, the lower her leptin levels, so the more she eats, and the heavier she gets. Hypocretin Neurons may serve as one of the answers to the question of exactly how that phenomenon comes about. Or at least it plays a role. Because 1) Hypocretins simultaneously stimulate appetite and wakefulness, particularly through orexigenic output of the melanocortin system, and subsequent release of CRH, which activates the stress response, and 2) while Hypocretin Neurons wake us up, they also need to be quiet enough for people to go to sleep.
Finally, I raise the questions: how many disordered eaters have trouble sleeping? How many anorexics, binge eaters, calorie restrictors, exercise-addicts, stressed-out individuals, and very low-carb dieters have trouble sleeping? How many people try intermittent fasting and find that it disrupts their sleep or circadian rhythms? How many people wake up in the middle of the night or early in the morning, even though they still need sleep, but for the life of them feel so awake? Part of that answer lies in blood sugar metabolism, for sure. And in other places. Sleep is a hell of a complex phenomenon. But here– Hypocretin Neurons can become overburdened by excitatory signals. They get hyped up in the face of both decreasing leptin levels and leptin insensitivity. They are upset by restriction, and they are upset by fasting. Hypocretin Neurons demonstrate why so many people have difficulty with their appetite and their sleep. If you find that fasting disturbs your sleep, or that you are suffering disordered circadian rhythms along with stress or appetite problems, do you best to relax your system. Don’t fast. Relax. Exercise less. Reduce stress. Eat more. Put on weight. Eat more carbohydrates. Don’t graze. Increase your leptin sensitivity. And listen to your body.
Coming up next: nighttime eating syndrome, and how it’s all related.