.png)
The low-carb diet trend has really taken the wellness industry by storm over the past few years. Promising everything from weight loss to improved insulin sensitivity, longevity to improved cognitive function, the allure to ditch all carbs pulls you in with high hopes of resolving all your health issues. In this article I will go through my own experience with low carb dieting, as well as take a deeper look into the research and why I now believe this is a suboptimal way of eating for humans.
My low-carb experience
When I was in university, the ‘Banting’ diet, popularised by Tim Noakes, was becoming very popular in South Africa. At the time I was struggling with insulin-resistant PCOS and decided to give the low-carb diet a try after reading much of the promising research that low-carb diets could reverse insulin resistance.
I noticed improvements in my well-being in the first two years of eating this way. I lost a bit of weight, started feeling more energized, and noticed an enhanced ability to concentrate. However, my menstrual cycle continued to be erratic and was starting to become less and less regular.
I was so drawn into the world of primal/paleo/keto as more and more health experts were preaching this diet for optimal health, that I didn’t take serious note of the slow decline that was starting to happen in my health. I started experiencing restless leg syndrome, eczema, thinning hair, amenorrhea, poor quality sleep, and major mood ups and downs.
It only hit me that I had to make a serious change when I started becoming more serious about wanting to have a baby soon. I knew I had to get my hormone health in check and started searching for answers. I did some bloodwork and saw that my T3 was at a subclinical hypothyroid level. Feeling at a complete loss for answers, I finally came across the pro-metabolic community and the research of Dr. Ray Peat.
After slowly reintroducing carbs into my diet and putting a larger focus on optimizing my micro-nutrient intake, I have managed to restore a regular menstrual cycle and improve my thyroid health. I have now worked with many ladies who have also suffered through the risks associated with low-carb diets and have finally found optimal health with a tailored pro-metabolic meal plan that works for them.
The problems with a low carb diet
Elevation of stress hormones
Maintaining adequate glucose levels in the blood is necessary for survival. This is because glucose is needed by your cells for cellular respiration to occur. Cellular respiration is a set of metabolic reactions and processes that take place in your cells to convert food and oxygen into adenosine triphosphate (ATP). ATP is what fuels all your cellular processes.
Maintaining adequate blood glucose is so important that when your body does not receive the glucose it needs from food, it will secrete stress hormones (noradrenaline, adrenaline, cortisol, and glucagon) to stimulate lipolysis (to make more fatty acids available), glycogenolysis (the breakdown of glycogen for fuel) and gluconeogenesis (the production of glucose from amino acids, lactate, and glycerol) to keep blood sugar stable and provide your body with fuel.
This is an incredible survival mechanism your body has in order to sustain you during times of low glucose availability. However, when glucose doesn’t become available over longer periods of time, these hormones must stay high to continue to provide fuel.
This stress response helps to explain some of the initial benefits seen on a low-carb diet – because running on stress hormones feels pretty great in the short term! Heightened concentration, more energy, and weight loss can indeed occur when you have cortisol and adrenaline pumping through your system.
The problem is that your body can only continue to produce stress hormones for so long. Eventually, your ability to produce stress hormones becomes impaired. Because thyroid hormone is required to produce these hormones and cortisol suppresses your thyroid function by blocking the conversion of thyroid hormone by your liver. Eventually, you’ll reach a point where you can’t produce enough stress hormones to meet the demands of what your body needs in order to compensate. That’s when the real damage happens. When your body fails to compensate, physical degradation begins to occur.
Some argue that once you are ‘keto-adapted’, the stress response normalizes, and cortisol isn’t higher than normal. However, multiple studies have shown that cortisol is higher on a low-carb diet [1]– [4]. In addition to the stress hormones needed to liberate free fatty acids from your stored fat tissue to turn into energy and ketones, having excessive free fatty acids (FFA) in the bloodstream is itself a signaling molecule that you are undergoing stress, causing even more stress in the body [5].
Low thyroid function
There’s an abundance of research showing that low carb diets result in a fall in active T3 thyroid hormone, a rise in the thyroid blocking reverse T3 hormone, and fall in metabolic rate and energy production [6]– [9]. Thyroid function is one of the main determinants of health, as thyroid hormones regulate key bodily functions such as cellular respiration, heart rate, thermogenesis, electrolyte retention, and the conversion of cholesterol into steroid hormones.
Low-carb diets directly deplete liver glycogen and over-activate your adrenal glands. This increases cortisol production, which suppresses your thyroid function by blocking the conversion of thyroid hormone by your liver. Low-carb diets also result in high levels of circulating fats in the bloodstream. This suppresses your thyroid function by blocking your cells from using thyroid hormone.
Electrolyte issues
The importance of supplemental electrolytes while on a low-carb diet is well known. However, it isn’t just the amount of electrolytes you get in your diet that is important, but also your ability to retain electrolytes.
Insulin plays a very important role in electrolyte retention. Insulin often gets vilified in the low-carb space. However, insulin is a very necessary hormone for humans. The signaling of insulin is critical at the level of the kidney for proper maintenance of electrolytes [10]. If you are chronically low-carb and are not having any post-meal rise in insulin, your body will waste sodium. That is because insulin is an antinatriuretic, i.e. insulin is connected with the conservation of sodium.
This explains the electrolyte deficiency symptoms many start to experience over time on a low-carb diet, e.g., heart palpitations, muscle cramping, restless leg syndrome, and poor sleep quality. No amount of supplemental electrolytes will fix the electrolyte deficiencies people see on a low-carb diet.
Long term effects on blood sugar regulation
When glucose is restricted in the diet, cortisol, and glucagon stimulate gluconeogenesis, which creates glucose to prevent hypoglycemia. Insulin is a cortisol antagonist, meaning that when insulin remains low, cortisol keeps increasing. Cortisol in turn inhibits insulin secretion and over time, progressively higher cortisol and more gluconeogenesis eventually lead to hyperglycemia [11]– [13].
Low carb advocates claim that this diet improves insulin sensitivity. However, studies have shown that improvements in insulin resistance are short-lived [14], [15], and a long-term keto diet can actually worsen insulin resistance [16]– [19].
Hormonal decline
Many women have experienced irregular menstrual cycles on a low-carb diet, and some even a complete loss of their cycle (amenorrhea). As we’ve discussed, a low-carb diet can suppress thyroid function, and adequate thyroid function is needed to convert cholesterol to sex hormones. In addition, proper blood sugar regulation is essential to regulate hormone health.
Dr. Katharina Dalton, a PMS and progesterone researcher, states in her book Once a Month:
"Progesterone receptors cannot transport or bind to, a molecule of progesterone if there has been a drop in blood sugar"
"Progesterone receptors do not transport progesterone molecules into the nucleus of cells if adrenaline is present"
"We must have a stable blood sugar level, and for that, we insist that patients use the three-hourly starch diet. The ideal is that they should eat in a way that does not cause a drop in the blood sugar because a drop in the blood sugar will stop the utilization of progesterone for seven days"
Men also often experience a decrease in sex hormones on a low-carb diet. There are several studies that show that lower carbohydrate intake decreases testosterone over time. In this paper, they suggest that “reduced availability of glucose may be responsible for decreased testosterone synthesis or hypoandrogenism in the testis” [20].
In conclusion
I believe that it is important to remain open and curious about nutrition research and never become dogmatic in your thinking. I was absolutely sold on the low carb benefits for years but now believe that carbohydrates are essential to living a thriving life. As a curious nutrition nerd, I will continue to stay up to date with the latest low-carb research and adjust my viewpoints if new evidence comes to light. But at the end of the day, research will never be as good of an indicator of a diet’s effectiveness as to how you feel.
I encourage you to keep checking in with yourself. Re-evaluate if your current diet is working for you. Do you:
Have consistent energy all day long
Sleep soundly through the night
Have a healthy sex drive
A regular and pain-free menstrual cycle
Poop every day
Maintain a warm body temperature (above 36.5 degrees Celsius)
Have strong hair and nails with clear skin
Experience emotional stability
If you lose a lot of weight eating a certain way but end up with thinning hair, low libido, and a horrible mood, is that really an optimal diet?
References
[1] C. B. Ebbeling et al., “Effects of dietary composition on energy expenditure during weight-loss maintenance,” JAMA - Journal of the American Medical Association, vol. 307, no. 24, 2012, doi: 10.1001/jama.2012.6607.
[2] R. H. Stimson et al., “Dietary macronutrient content alters cortisol metabolism independently of body weight changes in obese men,” Journal of Clinical Endocrinology and Metabolism, vol. 92, no. 11, 2007, doi: 10.1210/jc.2007-0692.
[3] E. P. Widmaier, J. Margenthaler, and I. Sarel, “Regulation of pituitary-adrenocortical activity by free fatty acids in vivo and in vitro,” Prostaglandins, Leukotrienes and Essential Fatty Acids, vol. 52, no. 2–3, 1995, doi: 10.1016/0952-3278(95)90019-5.
[4] V. J. Miller, F. A. Villamena, and J. S. Volek, “Nutritional ketosis and mitohormesis: Potential implications for mitochondrial function and human health,” Journal of Nutrition and Metabolism, vol. 2018. 2020. doi: 10.1155/2018/5157645.
[5] R. R. Wolfe, J. H. Shaw, and M. J. Durkot, “Energy metabolism in trauma and sepsis: the role of fat.,” Prog Clin Biol Res, vol. 111, 1983.
[6] E. Molteberg et al., “Effects of modified Atkins diet on thyroid function in adult patients with pharmacoresistant epilepsy,” Epilepsy and Behavior, vol. 111, 2020, doi: 10.1016/j.yebeh.2020.107285.
[7] E. Kose, O. Guzel, K. Demir, and N. Arslan, “Changes of thyroid hormonal status in patients receiving ketogenic diet due to intractable epilepsy,” Journal of Pediatric Endocrinology and Metabolism, vol. 30, no. 4, 2017, doi: 10.1515/jpem-2016-0281.
[8] R. G. Hendler, M. Walesky, and R. S. Sherwin, “Sucrose substitution in prevention and reversal of the fall in metabolic rate accompanying hypocaloric diets,” The American Journal of Medicine, vol. 81, no. 2, 1986, doi: 10.1016/0002-9343(86)90264-0.
[9] F. Fery, P. Bourdoux, J. Christophe, and E. O. Balasse, “Hormonal and metabolic changes induced by an isocaloric isoproteinic ketogenic diet in healthy subjects,” Diabete et Metabolisme, vol. 8, no. 4, 1982.
[10] S. Tiwari, S. Riazi, and C. A. Ecelbarger, “Insulin’s impact on renal sodium transport and blood pressure in health, obesity, and diabetes,” American Journal of Physiology - Renal Physiology, vol. 293, no. 4. 2007. doi: 10.1152/ajprenal.00149.2007.
[11] A. Kamba et al., “Association between higher serum cortisol levels and decreased insulin secretion in a general population,” PLoS ONE, vol. 11, no. 11, 2016, doi: 10.1371/journal.pone.0166077.
[12] N. H. F. Fine et al., “Glucocorticoids reprogram b-cell signaling to preserve insulin secretion,” in Diabetes, 2018, vol. 67, no. 2. doi: 10.2337/db16-1356.
[13] J. H. Ellenbroek et al., “Long-term ketogenic diet causes glucose intolerance and reduced β- and α-cell mass but no weight loss in mice,” American Journal of Physiology - Endocrinology and Metabolism, vol. 306, no. 5, 2014, doi: 10.1152/ajpendo.00453.2013.
[14] G. D. Foster et al., “A Randomized Trial of a Low-Carbohydrate Diet for Obesity,” New England Journal of Medicine, vol. 348, no. 21, 2003, doi: 10.1056/nejmoa022207.
[15] J. Z. Goldenberg et al., “Efficacy and safety of low and very low carbohydrate diets for type 2 diabetes remission: systematic review and meta-analysis of published and unpublished randomized trial data,” BMJ, vol. 372, 2021, doi: 10.1136/bmj.m4743.
[16] K. P. Kinzig, M. A. Honors, and S. L. Hargrave, “Insulin sensitivity and glucose tolerance are altered by maintenance on a ketogenic diet,” Endocrinology, vol. 151, no. 7, 2010, doi: 10.1210/en.2010-0175.
[17] L. Crosby et al., “Ketogenic Diets and Chronic Disease: Weighing the Benefits Against the Risks,” Frontiers in Nutrition, vol. 8. 2021. doi: 10.3389/fnut.2021.702802.
[18] J. Kong et al., “Longitudinal changes in insulin resistance in children with epilepsy on ketogenic diet: Prevalence and risk factors,” Epilepsy and Behavior, vol. 112, 2020, doi: 10.1016/j.yebeh.2020.107393.
[19] E. L. Goldberg, I. Shchukina, J. L. Asher, S. Sidorov, M. N. Artyomov, and V. D. Dixit, “Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue,” Nature Metabolism, vol. 2, no. 1, 2020, doi: 10.1038/s42255-019-0160-6.
[20] A. Banerjee, Anuradha, K. Mukherjee, and A. Krishna, “Testicular glucose and its transporter GLUT 8 as a marker of age-dependent variation and its role in steroidogenesis in mice,” Journal of Experimental Zoology Part A: Ecological Genetics and Physiology, vol. 321, no. 9, 2014, doi: 10.1002/jez.1881.
Comments