In the first post I wrote on the physiology of women’s weight loss, I focused on the role estrogen plays in fat stores. I noted at the end of the post that estrogen is involved with sending appetite-regulating signals to the brain. This is an important factor in female weight loss. Men have hormonal feedback that dictates their satiation, too, but their body is less attached to how much fat it has. For a woman, having fat is crucial for pregnancy and childbirth. For this reason, a woman’s body errs on the side of caution with respect to fat stores. When in doubt, it screams “eat!”
What this means is that it is much easier for women to be barraged with physiological demands to eat. These drives are not malicious things, and a woman can never be upset with her body for having them. It’s natural, and it’s necessary for health. Only by accepting our strong biological need for food as physiological fact can we women truly move forward with love, holistic healing, and positive, even pleasurable weight loss.
What follows below is an overview of the mechanisms by which women’s bodies “hang on” to fat stores. This is not to say that the body wants to be overweight. The body actually wants to be a proper, fit, attractive weight. What happens is that normal weight-regulating factors get dysregulated by an inflammatory diet, and prolonged abuse drives a system further and further off-track. The good news is that because a woman’s body wants to be an appropriate weight, once the woman starts treating her body with proper love and nourishment, the pounds naturally slide off.
Fat as a vital organ
Not too long ago, scientists thought that fat cells were simple units of energy storage. Metabolism would grab the energy stored in the fat cells when it needed it, and then the fat cells would continue lying there inert. Metabolism might deposit more energy into them at another time, and then later it would come grab the energy back. Fat cells were considered storage units, and not anything more.
Since 1994 with the discovery of leptin, science has gradually unearthed the surprising notion that fat tissue is not just a storage space but is also an endocrine organ in and of itself. Fat receives signals from hormones; it is actively involved in how much fat gets stored within its own reserves, and how; and it sends out potent signals of its own. These signals are crucial. They tell the brain how much energy is currently being stored in the form of fat. Higher levels of leptin signal to the hypothalamus that an organism does not need to eat anymore. Potent appetite stimulators such as neuropeptide Y and anandamide are inhibited by leptin in the hypothalamus, and the production of alpha-MSH, an appetite suppressant, is encouraged. Though there are dozens of hormones and neurotransmitters involved in signalling appetite to and from the brain, what this demonstrates is that leptin more or less runs the show. More leptin = less eating.
That is, unless the organism is leptin resistant.
Leptin resistance occurs when leptin has flooded a system. In addition to originating in fat stores, leptin levels in the blood rise with food consumption. Leptin 1) spikes after consumption of a large meal, particularly a carbohydrate-heavy meal, since leptin works in tandem with insulin, and 2) it sort of dribbles into the bloodstream if food is eaten in smaller quantities throughout the day. So leptin levels rise whenever the body really thinks it has been well-fed.
Over-secretion of leptin is the primary means by which people dysregulate their leptin signalling, for example, if they eat too many meals without waiting for hunger to return in between them, or if they graze on food all day, or if they have a couple of snacks each day. Basically, leptin resistance develops when normal weight-regulating drives are ignored. This is easy to do in the presence of highly palatable food and drink. Other factors that can throw someone’s leptin signals under a bus are stress, loss of sleep, problems with neurotransmitters, or nutrient deficiencies. Under the influence of these factors, or perhaps several of them in conjunction, it becomes difficult for a woman to hear the leptin signalling in her hypothalamus.
Once people begin ignoring their leptin signals, they get easier and easier to ignore. This is because constantly elevated leptin levels cause leptin receptors to become insensitive to the leptin floating around in the bloodstream. Then, as the body realizes that it’s normal leptin signalling isn’t getting the job done, it incites more eating, more weight gain, and higher leptin levels in hopes that an increased leptin signal will get through. For this reason, obesity is correlated with high leptin levels, even though many obese people complain of constant hunger.
Leptin resistance is a problem for everybody. Both men and women. Without fixing leptin sensitivity problems, it’s very difficult to lose weight, and it’s even more difficult to enact any kind of dietary restriction. But women, who have higher levels of leptin than men (having higher body fat percentages) and who have HPA axes more attuned to energy conservation, are particularly sensitive to fluctuations in leptin levels.
Leptin and menstruation
Achieving a certain leptin level is the primary trigger for menarche (the first incidence of menstruation) Stress, genetics, being exposed to smoking, and not being breast fed are other important factors. So far as researchers can tell, throughout evolutionary history a woman’s period likely started around 15 or 16 years of age. A few studies were conducted in the nineteenth century documenting menarche. In 1850, girls began menstruating at an average age of 17; by 1960 that age decreased to 13 years old. Today in America, approximately ten per cent of girls start to menstruate before 11 years of age, and ninety per cent of all US girls are menstruating by 13.75 years, with a median age of 12.43 years. Both black and latino girls begin menstruating before white girls.
Many suspect that the higher body weights and higher leptin levels are responsible for the change in menarche. A 2011 study found that each 1 kg/m2 increase in childhood BMI can be expected to result in a 6.5 per cent higher risk of menarche before reaching 12 years of age.
Leptin and the reproductive set point
Knowing about puberty and menarche is so important for adult women because a woman’s reproductive functioning for the rest of her life is influenced by the conditions of her early reproductive years. Having started menstruation with a certain leptin concentration in the blood, a woman’s body treats this as a “set point ” of sorts later on. Having had a certain level of leptin, too, influences the young girl’s estrogen and progesterone levels, such that these also become reproductive set points. Therefore, if a woman drops too far below her set leptin or estrogen levels later in life by losing too much weight, her body will do its damndest to get those levels back up. A similar phenomenon happens if she becomes overweight and leptin resistant.
Stimulating appetite in response to low leptin levels
The way a body tries to increase leptin and estrogen concentrations is to increase fat mass. The way to increase fat mass is to increase appetite. This is why leptin is such a potent signal in a woman’s brain. With decreased leptin levels (or leptin insensitivity), appetite-stimulating neurons up-regulate powerfully.
Importantly, more women profess sugar addiction than men. One of the neurons that detects decreasing leptin concentrations in the blood is called Neuropeptide Y. Neuropeptide Y stimulates carbohydrate craving. Women who are experiencing starvation– or at least women who’s hypothalama are detecting lower leptin levels than their bodies think are optimal — experience insidious carbohydrate cravings.
Are women stuck in leptin set points?
No. Not necessarily.
The thing is, it’s complicated. A woman’s body will never “want” to be overweight. Women start menstruating at a certain leptin level and at a certain age, but even if this occurs at a very young age, the leptin is still around the same absolute level that another woman might experience, just many years earlier. So her leptin levels, if higher earlier than optimal, still are not shooting through the roof at menarche.
Moreover, if a young girl is overweight when she starts her period, at that time her body is probably fighting for and signalling a desire to lose weight. It’s just not working because some of the signals have been disturbed by poor diet and lifestyle. This woman’s body’s need for and desire to lose weight will persist for the rest of her life. The hormone and appetite pathways are all still in place. They are just begging to be restored to their normal function. All the woman needs to do is listen, and to nourish her body properly. In this way, it will be her partner in weight loss, rather than her adversary.
Other appetite stimulators
Appetite is stimulated via a few other important pathways. They are not limited to women. For example, an individual’s cravings for certain foods increases as a result of nutrient deficiencies. Fluctuating insulin and blood sugar are important. Stress is important. Social conditioning, negative thought patterns, psychological responses to hardship, and body image issues also powerfully stimulate cravings.
Neurotransmitters as appetite stimulators
Perhaps most significant, however, is the relationship between neurotransmitters and food, specifically for women. When serotonin levels drop, cravings, again, particularly for carbohydrates, increase. Serotonin levels can be disrupted by a vast number of problems. These span from nutrient deficiencies to an omega 6 – omega 3 imbalance to poor sleep to obesity to exercise and to stress. Serotonin levels also fluctuate with the menstrual cycle. A drop in serotonin during the luteal phase (the last two weeks) of the menstrual cycle is thought to be by many the dominant cause of PMS. This would explain why many women experience increased cravings for sweets throughout PMS. These are natural, up to a point. But PMS is an extreme fluctuation, and solving the underlying diet and lifestyle factors causing PMS should also decrease the wild swings in cravings that many women suffer throughout their menstrual cycles.
The role of neurotransmitters in appetite deserves several posts of its own. They are forthcoming. For now, it suffices to note that neural mood regulators are strong links between a woman’s reproductive system and her weight regulation mechanisms. Sub-optimal serotonin levels in particular increase carbohydrate cravings.
All that said…
Women come equipped with a system designed to maintain adequate fat mass. If a woman is overweight, it’s because the normal weight regulators she has in place are not receiving the proper nourishment required for effective signalling. Leptin insensitivity, in the case of an overweight woman, or low leptin levels, in the case of an underweight woman, compel her to eat and to eat and to eat. Estrogen, as I noted in a previous post, is also a significant weight-regulator unique to women. It, too, is disrupted with diet and lifestyle. Therefore, with the restoration of the proper functioning of all of the underlying mechanisms at work in a woman’s body, specifically with leptin and with estrogen levels, a woman’s weight can slide off. More on that in my upcoming post on the easiest, most natural way (paleo diet! decreased stress! self-love!) for women to lose weight.