Hormonal issues become more common as you age, and while men do experience the effects of hormonal changes, women tend to be affected to a greater degree. A ketogenic diet has a somewhat unique impact on hormones, as well as the thyroid, menstruation cycles, and the HPA axis. In this article, we will cover this impact, as well as the effect keto has on hormones like cortisol. Using this information, you can make the appropriate adjustments to your diet and lifestyle – to truly improve your health.
What Is the Keto Diet?
The keto diet — also referred to as the ketogenic diet — is a low-carbohydrate diet, where your body uses fat for fuel. By removing almost all carbohydrates, and inserting healthy fats in their place, your body enters an advanced fat-burning condition called nutritional ketosis. Once in ketosis, your body will start using fat for energy, rather than carbohydrates or glucose.
There are a number of ways to shift into nutritional ketosis. The most important is cutting out the carbs. The standard American diet recommends consuming between 200 and 300 grams of carbohydrates per day. By contrast, keto usually involves eating 20 grams of carbohydrates throughout the day. While the keto diet is certainly high in healthy fats – cutting the carbs is actually the most critical step to getting in (and staying in) ketosis. Before we dive into specifics, we need to understand exactly how keto works.
How the Keto Diet Works
In a normal American diet, carbohydrates are consumed in abundance. Once eaten, carbs turn into glucose. Glucose can be thought of as the simplest form of sugar, and it is easy for the body to convert and use as your primary source of energy. Thus, glucose is your main source of fuel, at least when consuming the standard American diet. As a lot of carbs are consumed, your body has a rise in blood sugar, as these carbs are turned into glucose. Then, your body creates insulin, which is a hormone meant to transport glucose throughout your body. You may have heard the term ‘insulin spike’ – this is what that term refers to.
As your body uses this glucose, any extra is stored. This reserve of energy sounds good – until you release its stored as body fat. If you keep eating carbohydrates, your body will continually use glucose as its fuel source. This may seem beneficial, but in reality, it means you can’t dip into your fat stores. This leaves you in a state of constantly storing excess energy, which leads to weight gain. Meanwhile, you are unable to dip into your fat stores, so you can’t burn off any fat.
But luckily for those who follow the keto diet, the only way to start burning off those fat stores, is by removing carbohydrates entirely. In turn, this diminishes your glucose stores (usually called ‘glycogen’). At this point, your body essentially realizes it is running out of energy, so it starts dipping into its reserves of fat. And there you have it – how keto burns off your stored body fat, and ramps up your metabolism.
Keto and Your Thyroid
There is a huge amount of misinformation out there about a keto diet’s impact on your thyroid. The truth is, keto lowers T3, which is the thyroid marker hormone. T3 is in some ways working against your body at higher levels, as it causes your cells to use more energy. Hence, a reduction in T3 is beneficial. Scientists think that a lowering of T3 will reduce free radical production and may even lead to a longer life. T4 is another important part of thyroid function, and it works with T3 to keep your body temperature, heart rate, and metabolism in proper ranges. Again, it is easy to see why the misinformation is out there, but the truth is far different. Keto positively impacts your thyroid, as well as positively impacting nearly every relevant biomarker of your health.
Keto and Cortisol
Cortisol is the body’s ‘stress hormone,’ and while it is commonly perceived in a negative light, it actually performs many helpful tasks which are essential for the body. For example, when you need to do an intense workout, cram for an important exam, or if you have to ward off a burglar – cortisol is critical for these processes to happen. However, it is easy to see how too much of this hormone could cause problems. You don’t always want to be on the edge of excess energy – for starters, how would you sleep? Cortisol dysregulation is a root cause of many health problems, and it’s important that you keep your cortisol in check, if you want to be optimally healthy. A keto diet is high in good fats, and moderate in protein, which makes your cortisol happy. By not having peaks and valleys of sugar rushes and crashes, your body is better able to stay in homeostasis.
Keto and Your Exercise Routine
Following a good exercise routine is required for any positive health outcomes, and keto is no different. But when it comes to hormonal issues, it is also easy to go too far into the red, and exercise too much. If you overtrain, you can quickly throw your hormones out of whack – especially cortisol. The most common occurrence as it relates to keto is attempting to do high-intensity interval training (HIIT) too often. If you are in ketosis, doing HIIT more than three times per week may do you more harm than good. Just as your body needs exercise, your body also needs rest.
Keto and the HPA Axis
The hypothalamic-pituitary-adrenal axis is critical for your overall health. You can think of the HPA axis as the nexus of the universe, at least in terms of your internal health. The hypothalamus puts out hormones and works with the adrenal and pituitary glands to keep everything running smoothly. When you start following a ketogenic diet, you may find an improvement with HPA axis function, as the data shows keto may improve hypothalamic stimulation. Other interesting research shows that ketosis may actually use a different metabolic pathway than normal glucose signaling, which may be part of why the keto approach is so effective. Hypothalamic neuropeptides are also elevated when following a keto diet, which means your HPA axis should be humming along smoothly – as long as you stay in ketosis.
Keto and Undereating
Perhaps surprisingly, there are many keto dieters who simply do not eat enough. This is likely due to the hunger blunting effects of the diet. It is important to track your calories when you first start the keto approach, to make sure you are giving your body what it needs. If you are not used to eating a diet low in carbs and high in fat, you will likely feel full when your body still needs more calories. Another potential problem with undereating comes from intermittent fasting (IF). While fasting is a great way to optimize your health, you cannot do it every day. It’s simply too much stress on your hormones and body. It is imperative that you track your food intake aggressively when you practice intermittent fasting. And be sure not to overdo it – think about the long term, not the short term.
Keto and Your Period
The menstrual cycle is a fickle thing. There are many, many different factors that can impact your period, as well as your premenstrual symptoms (PMS). Keto has actually been shown to have positive impacts on your period. In some cases, if you’ve had irregular periods for a long amount of time, you may find yourself getting back into a normal menstrual cycle when following a ketogenic diet. Some keto dieters also report increased flow, but this typically only happens in the beginning stages of adopting the diet. Once your body adapts to keto, things should go back to normal. The bottom line is that a ketogenic diet should only have a positive impact on your period. If you are experiencing issues with your menstrual cycle, consult with your doctor immediately, as it is likely that there are more serious issues going on.
A keto diet should positively impact your hormones – not negatively impact them. Scientific research has shown benefits for thyroid health, as keto helps to lower T3 levels. With this lowered level, you can function better, as well as reduce free radical production. You may even live longer as a result. Scientific data has also shown cortisol levels drop when following a proper ketogenic diet. While cortisol is a very necessary hormone, it must stay in safe ranges. Ketosis helps to make this happen – and it also does a great job at helping you achieve other health goals.
The keto approach has a positive impact on your weight and fat loss goals, and can even lead to incredible physical and mental changes. However, it is important to not overtrain. You must exercise smartly, as well as eat responsibly, for truly optimal health outcomes. A ketogenic approach helps to keep your HPA axis in an optimal range, and actually may improve its overall functioning. If you are following keto, it is also crucial to make sure you are consuming enough calories. Undereating typically results in poor hormonal results, and can also lead to a laundry list of other health problems. A keto diet also has positive impacts on your menstrual cycle. If you believe you are experiencing hormonal issues of any kind, it is important to consult with your doctor.
The Best Way to Measure Your Ketones
Until now, there has not been a convenient and reliable way to check your ketones. That’s why we invented the first and only clinically- backed ketone breath monitor. By simply breathing in our device, you will have a reliable measurement of your current ketone levels in seconds, allowing you to track ketone changes all day. No more urine strips, no more pricking your finger – just a fast, easy and reliable breath test. You can bring our device with you to the office, take it to the gym – you can truly check your ketones anywhere. Unlike previous devices, which were often poorly made, unreliable, and not backed by clinical research – our ketone breath monitor has a patented deep lung sampling technique, a requirement for accuracy.. This means no other device is legally allowed to use our exclusive technology. Whether you are brand new to keto and want a convenient and reliable way to check your ketone levels, or you’re an elite level biohacker – Biosense is the perfect way to measure your ketones.
You don’t need to worry about continually buying strips, continually pricking your finger – we have all you need, in just one device. One of our favorite features is the personalized insights you get with the device. Every time you measure, your results are graphed and stored, so you can easily track your progress. Until now, there has not been an easy and convenient way to check your ketone levels – which has made many people give up on the keto diet entirely. But that outcome is no longer necessary, as we’ve made a device that does all the work for you. Just simply take one breath into the device, and within seconds you’ll know your ketone level. Whether your goal is to burn fat, lose weight, or improve your blood sugar – we have the answer.
Gaskins AJ, Mumford SL, Zhang C, Wactawski-Wende J, Hovey KM, Whitcomb BW, Howards PP, Perkins NJ, Yeung E, Schisterman EF. Effect of daily fiber intake on reproductive function: the BioCycle Study. Am J Clin Nutr 2009;90:1061–9.
Austin GL, Ogden LG, Hill JO. Trends in carbohydrate, fat, and protein intakes and association with energy intake in normal-weight, overweight, and obese individuals: 1971–2006. Am J Clin Nutr 2011;93:836–43.
Behre HM, Kuhlage J, Gassner C, Sonntag B, Schem C, Schneider HP, Nieschlag E. Prediction of ovulation by urinary hormone measurements with the home use ClearPlan Fertility Monitor: comparison with transvaginal ultrasound scans and serum hormone measurements. Hum Reprod 2000;15:2478–82.
Patterson RE, Kristal AR, Tinker LF, Carter RA, Bolton MP, Agurs-Collins T. Measurement characteristics of the Women’s Health Initiative food frequency questionnaire. Ann Epidemiol 1999;9:178–87.
Gann PH, Kazer R, Chatterton R, Gapstur S, Thedford K, Helenowski I, Giovanazzi S, Van Horn L. Sequential, randomized trial of a low-fat, high-fiber diet and soy supplementation: effects on circulating IGF-I and its binding proteins in premenopausal women. Int J Cancer. 2005;116(2):297–303.
Kaaks R, Bellati C, Venturelli E, Rinaldi S, Secreto G, Biessy C, Pala V, Sieri S, Berrino F. Effects of dietary intervention on IGF-I and IGF-binding proteins, and related alterations in sex steroid metabolism: the Diet and Androgens (DIANA) Randomised Trial. Eur J Clin Nutr. 2003;57(9):1079–1088.
Maskarinec G, Takata Y, Kaaks R. The relation between nutritional factors and insulin-like growth factor-I in premenopausal women of different ethnicity. Eur J Nutr. 2005;44(2):105–113.
Hu FB, Stampfer MJ, Manson JE, et al. Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med. 1997;337(21):1491–1499.
Wolk A, Manson JE, Stampfer MJ, Colditz GA, Hu FB, Speizer FE, Hennekens CH, Willett WC. Long-term intake of dietary fiber and decreased risk of coronary heart disease among women. JAMA. 1999;281(21):1998–2004.
Golay A, DeFronzo RA, Ferrannini E, et al. Oxidative and non-oxidative glucose metabolism in non-obese type 2 (non-insulin dependent) diabetic patients. Diabetologia. 1988;31:585–91.
Defronzo RA, Simonson D, Ferrannini E. Hepatic and peripheral insulin resistance: A common feature of type 2 (non-insulin-dependent) and type 1 (insulin-dependent) diabetes mellitus. Diabetologia. 1982;23:313–9.
Defronzo RA, Diebert D, Hendler R, Felig P. Insulin sensitivity and insulin binding in maturity onset diabetes. J Clin Invest. 1979;63:939–46.
Pilkington TR, Rosenoer VM, Gainsborough H, Carey M. Diet and weight-reduction in the obese. Lancet. 1960;i:856–8.
Howard BV, Wylie-Rosett J. Sugar and cardiovascular disease: A statement for healthcare professionals from the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation. 2002;106:523–7. Erratum in 2003;107:2166.
Franceschi S, Favero A, Decarli A, et al. Intake of macronutrients and risk of breast cancer. Lancet. 1996;347:1351–6.
Liu S, Manson JE, Stantpfer MJ, et al. Dietary glycemic load assessed by food-frequency questionnaire in relation to plasma high-density-lipoprotein cholesterol and fasting plasma triacylglycerols in postmenopausal women. Am J Clin. 2001;73:560–6.
Gaziano JM, Hennekens CH, O’Donnell CJ, Breslow JL, Buring JE. Fasting triglycerides, high-density lipoprotein and risk of myocardial infarction. Circulation. 1997;96:2520–5.
Kreitzman SN. Factors influencing body composition during very-low-caloric diets. Am J Clin Nutr. 1992;56(l Suppl):217S–23S.
Cullingford TE, Eagles DA, Sato H. The ketogenic diet upregulates expression of the gene encoding the key ketogenic enzyme mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase in rat brain. Epilepsy Res. 2002;49:99–107.
Prentice AM. Manipulation of dietary fat and energy density and subsequent effects on substrate flux and food intake. Am J Clin Nutr. 1998;67(3 Suppl):535S–41S.
Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med. 2003;348:2082–90.
He K, Merchant A, Rimm EB, et al. Dietary fat intake and risk of stroke in male US healthcare professionals: 14 year prospective cohort study. BMJ. 2003;327:777–82.
Westman EC, Mavropoulos J, Yancy WS, Volek JS. A review of low-carbohydrate ketogenic diets. Curr Atheroscler Rep. 2003;5:476–83.
Petersen KF, Befroy D, Dufour S, et al. Mitochondrial dysfunction in the elderly: Possible role in insulin resistance. Science. 2003;300:1140–2.
Foster-Powell K, Holt SH, Brand-Miller JC. International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr. 2002;76:5–56.
Leeds AR. Glycemic index and heart disease. Am J Clin Nutr. 2002;76:286S–9S.
Liu S, Willett WC, Stampfer MJ, et al. A prospective study of dietary glycaemic load, carbohydrate intake, and risk of coronary heart disease in US women. Am J Clin Nutr. 2000;71:1455–61.
Sims EA, Danford E, Jr, Horton ES, Bray GA, Glennon JA, Salans LB. Endocrine and metabolic effects of experimental obesity in man. Recent Prog Horm Res. 1973;29:457–96.
Hollenbeck B, Y-Di Chen, Reaven GM. A comparison of the relative effects of obesity and non-insulin dependent diabetes mellitus on in vivo insulin-stimulated glucose utilization. Diabetes. 1984;33:622–6.
Kolterman OG, Gray RS, Griffin J, et al. Receptor and postreceptor defects contribute to the insulin resistance in noninsulin-dependent diabetes mellitus. J Clin Invest. 1981;68:957–69.
Gresl TA, Colman RJ, Roecker EB, et al. Dietary restriction and glucose regulation in aging rhesus monkeys: A follow-up report at 8.5 yr. Am J Physiol Endocrinol Metab. 2001;281:E757–65.
Hansen BC, Bodkin NL. Primary prevention of diabetes mellitus by prevention of obesity in monkeys. Diabetes. 1993;42:1809–14.
Coulston AM, Liu GC, Reaven GM. Plasma glucose, insulin and lipid responses to high-carbohydrate low-fat diets in normal humans. Metabolism. 1983;32:52–6.
Chen YDI, Swami S, Skowronski R, Coulston AM, Reaven GM. Effects of variations in dietary fat and carbohydrate intake on postprandial lipemia in patients with non-insulin dependent diabetes mellitus. J Clin Endocrinol Metab. 1993;76:347–51.
Mitchell GA, Kassovska-Bratinova S, Boukaftane Y, et al. Medical aspects of ketone body metabolism. Clin Invest Med. 1995;18:193–216.
Koeslag JH. Post-exercise ketosis and the hormone response to exercise: A review. Med Sci Sports Exerc. 1982;14:327–34.
Winder WW, Baldwin KM, Holloszy JO. Exercise-induced increase in the capacity of rat skeletal muscle to oxidize ketones. Can J Physiol Pharmacol. 1975;53:86–91.
Yehuda S, Rabinovitz S, Mostofsky DI. Essential fatty acids are mediators of brain biochemistry and cognitive functions. J Neurosci Res. 1999;56:565–70.
Amiel SA. Organ fuel selection: Brain. Proc Nutr Soc. 1995;54:151–5.
Singhi PD. Newer antiepileptic drugs and non surgical approaches in epilepsy. Indian J Pediatr. 2000;67:S92–8.
Janigro D. Blood-brain barrier, ion homeostatis and epilepsy: Possible implications towards the understanding of ketogenic diet mechanisms. Epilepsy Res. 1999;37:223–32.
Kossoff EH, Pyzik PL, McGrogan JR, Vining EP, Freeman JM. Efficacy of the ketogenic diet for infantile spasms. Pediatrics. 2002;109:780–3.
El-Mallakh RS, Paskitti ME. The ketogenic diet may have mood-stabilizing properties. Med Hypotheses. 2001;57:724–6.
Ziegler DR, Araujo E, Rotta LN, Perry ML, Goncalves CA. A ketogenic diet increases protein phosphorylation in brain slices of rats. J Nutr. 2002;132:483–7.
Chen YD, Hollenbeck CB, Reaven GM, Coulston AM, Zhou MY. Why do low-fat high-carbohydrate diets accentuate postprandial lipemia in patients with NIDDM? Diabetes Care. 1995;18:10–6.
Gardner CD, Kraemer HC. Monosaturated versus polyunsaturated dietary fat and serum lipids and lipoproteins. Arterioscler Thromb Vasc Biol. 1995;15:1917–25.
Jeppesen J, Schaaf P, Jones C, Zhoue MY, Chen YD, Reaven GM. Effects of low-fat, high-carbohydrate diets on risk factors for ischemic heart disease in post-menopausal women. Am J Clin Nutr. 1997;65:1027–33.
Mensink RP, Katan MN. Effect of dietary fatty acids on serum lipids and lipoproteins. Arterioscler Thromb. 1992;12:911–9.
Groot PH, Van Stiphout WA, Krauss XH, et al. Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease. Arterioscler Thromb. 1991;11:653–62.
Patsch JR, Miesenbock G, Hopferweiser T, et al. Relation of triglyceride metabolism and coronary artery disease studies in the postprandial state. Arterioscler Thromb. 1992;12:1336–45.
Abbasi F, McLaughlin T, Lamendola C, et al. High carbohydrate diets, triglyceride-rich lipoproteins and coronary heart disease risk. Am J Cardiol. 2000;85:45–8.[/showhide]