At our next Fitter Food Academy, we’ll be talking about some of the key hormonal players involved in fat loss and health, with particular attention to those that govern appetite and satiety. Studies suggest there are some highly effective nutritional measures you can implement to improve the communication signals from these hormones in favour of healthy weight management.
You may not realise this but we are equipped with a highly effective homeostatic system to naturally control our levels of body fat. It’s designed to protect us from both over- and under eating and operates via a whole team of gastrointestinal hormones that control our appetite and satiety. However, one of the biggest challenges to this neat system is our modern day lifestyles packed with easily accessible, highly palatable, calorie-dense foods, lower levels of physical activity and highly stressful environments, this combination is railroading our hormonal feedback and effective management of body fat levels. The human body is simply not designed for a life of jelly babies, remote controls, granola, sofas, cars, crisps, living online and being stuck to a laptop.
We have covered insulin in previous blogs as one of the master hormones involved in the regulation of glucose metabolism in the body, however, leptin and a whole host of gut hormones are also working closely to manage your body fat stores by controlling hunger, satiety and cravings. Here’s a little insight into the systems in place that regulate body fat and appetite.
What never ceases to amaze me is this hormone was only discovered in 1994, yet it is literally the Big Fat Controller (excuse the pun!) of our body composition. Bless the 1980’s and its high fibre diets and funky leotards, we really had no clue what governed our fat mass. Leptin is secreted by our fat cells and circulating levels are proportional to our fat stores. It communicates directly with the hypothalamus in the brain and works by suppressing the appetite enhancing or ‘orexigenic’ processes and stimulating appetite lowering or ‘anorexigenic’ factors. Studies have explored administering leptin to rodents and observed a significant reduction in food intake, body weight and an increased energy expenditure. Leptin’s principle role is long-term regulation of energy balance, managing the amount of calories we consume and expend. It evolved to protect us from famine and also to prevent us from overeating which could equally compromise our chances of survival.
It is now known that people can be leptin deficient which can contribute towards obesity and weight management issues. Therapies administering leptin or leptin agonists (a chemical that binds to a hormone receptor site as leptin would do and activates it to produce the same biological response) are being explored as future tools against obesity-related diseases.
This is now believed to be the predominant biological abnormality in obese individuals. Significantly overweight people have large amounts of leptin circulating in their body but the brain is NOT receiving these signals so the body perceives itself to be starving and that no fat stores exist (remember fat cells produce leptin). Another mechanism whereby leptin resistance may occur is via an impairment in the transportation of leptin across the blood brain barrier.
The result of both of these is that the brain kicks into action, ordering you to eat more and up-regulates appetite hormones whilst lowering your metabolic rate, meaning you burn less calories at rest and feel constantly tired and lethargic. It’s worth noting that will power is almost futile in the face of this powerful hormone signaling.
We have covered insulin health in previous posts including improving insulin sensitivity and glucose metabolism. Insulin and leptin actually work very closely together in managing fat stores and energy expenditure in the body. Insulin stimulates the production of leptin from our fat cells and works on a similar feedback loop to the brain suggesting there’s a great deal on interaction between these two hormones. Similar to leptin, increased body fat stores results in decreased insulin sensitivity and a state of insulin resistance.
As insulin offers similar appetite regulating and body fat management capabilities as leptin the pharmaceutical industry are focusing efforts on developing drug interventions which improve insulin sensitivity. One of the most popular prescriptions is metformin used to treat obesity, adult onset diabetes and hormonal conditions like PCOS. Metformin promotes weight loss by suppressing the release of glucose from the liver and improving uptake and transportation into the cells for energy. There is still some question over the long-term effects of many pharmacological interventions and of course the cause of the hormone resistance must also be addressed. Plant based and natural formulas are now gaining more popularity including Berberine chloride, Chromium GTF, Gymmnestra and Alpha Lipoic Acid.
Whilst insulin and leptin regulate the on-going long-term signalling of your body fat status, a number of other hormones and factors act as daily meal initiators and terminators by governing our hunger and sense of fullness. The gastrointestinal-pancreatic system is actually the largest endocrine organ in the body and the following all play an essential role in deciding whether you actually feel you need to eat or need to stop.
Ghrelin is a hormone produced and released in the stomach and smaller amounts are produced by the small intestine, pancreas and brain. It increases hunger via a feedback mechanism to the hypothalamus region of the brain, crucial to the control of appetite. In scientific trials the administion of ghrelin to humans increased food intake by up to 30%. It has also been shown to act on a parts of the brain known as the amygdala that controls our sense of reward.
Ghrelin levels should be primarily regulated by food intake, they surge just before eating so regular meal patterns will be influential in deciding when ghrelin levels increase and the ‘hunger pangs’ kick in. Eating then reduces the concentration of ghrelin in the blood, interestingly it is thought carbohydrates and proteins restrict the release of ghrelin more than fats and in that sense are more satiating.
Ghrelin levels are often increased by dieting and severe calorie or macronutrient restriction. As mentioned before fighting hormonal instincts is almost impossible which is why many dietary solutions prove unsustainable as ghrelin levels are constantly rising and telling you EAT, EAT, EAT!
The Satiety Factors
There are also a number of mechanisms which function to prevent us from overeating by lowering appetite and making us feel full. These include:
- Cholecystokininm CCK
- Glucagon-like peptide (GLP)-1
- Oxyntomodulin (OXM)
- Peptide YY (PYY)
- Pancreatic polypeptide
CCK is the first gut hormone to affect appetite. Blood levels rise within 15 minutes of starting a meal (so take at least 15 minutes to eat your meals, ideally longer!) It is predominantly produced and released in the small intestine where it slows down the process of gastric emptying keeping you feeling full. Studies have investigated the possibility of drug therapies based on CCK as administration in trials encouraged people to reduce the size and duration of their meals, although it had little effect on weight loss as participants in the study simply decided to have more frequent meals so they could still have their cake and eat it 🙂
Glucagon-like peptide (GLP)-1
This peptide is released after eating in proportion to the calories ingested, animal studies have observed a reduction in food intake when GLP-1 is injected into the brain. It has been observed that obese individuals have lower levels of GLP circulating and do not seem to produce as much as lean individuals even after eating.
This is secreted alongside GLP-1 by the cells in the intestines after eating and also provides satiety signal. Studies have explored injecting OXM subcutaneously before eating into overweight and obese people over a 4-week period and resulted in a significant reduction in body weight.
Also secreted from intestinal cells with GLP-1 and OXM to indicate satiety. It has been suggested that obese individuals maybe in a state of PYY deficiency influencing their response to meals and meaning they have no ‘off’ switch. It’s worth noting studies have observed the minimisation of stress is vital to the effectiveness of PYY.
Pancreatic polypeptide (PP)
PP is released from the pancreas and colon, levels are at their lowest low when the body is in a fasted state and rise in proportionately to calorie intake. Animal studies have also observed PP administration may lead to an increase in energy expenditure and a reduction in body fat.
The Fitter Food Solution
As you’ve probably realised from the information the pharmaceutical industry is working fast and furiously to resolve the obesity crisis with medications that up regulate and down regulate these hormones and manipulate our natural biological processes back to how they should operate. The problem here is that unless we fundamentally change our nutrition and lifestyle these will only ever provide a temporary band aid as we are not addressing the underlying causes and drivers, you can also bet your life savings there will be side effects and consequences to the medications but that’s ok because they’ll be a drug to treat that too!
At our Fat Loss and Fuelling Health Academy we will be detailing how you can optimise your nutrition, use natural supplements and lifestyle modifications to re-sensitise hormornal activity improving the balance of appetite and satiety factors for healthy body fat regulation. Mindset and gut function also play an essential role and we’re delighted to have some guest speakers Coach Paul Watson and Naturopath Emma Mihill speaking on these topics.
Check out our conference agenda here.