Top 5 Diseases Keto Can Improve
Unless you’ve been in seclusion, you’ve probably heard some buzz about Keto from friends, family, co-workers and of course, the media. There are plenty of uninformed, skeptical sources who will tell you Keto is a fad or even dangerous for your health (we’ll dispel the myths around cholesterol and heart disease in our next post). What is often ignored are the numerous benefits ketosis has on vast array of disease (“link to what is a ketosis and a ketogenic diet”) and the positive impact it can have many aspects of your life: mood, energy, mental focus. We’re going dive a little further into the research and explore 5 common health ailments a ketogenic diet benefit.
Obesity: Lets break it down to the basics here. The CDC defines overweight or obese as a weight higher than is considered healthy for a given height (a). Body Mass Index (BMI) is a common tool used to help in this assessment, although it does have its flaws. For example, if you’re a dedicated weight-lifter and have a hefty amount of well-earned muscle mass and low body fat, you may very well have a high BMI implying obesity. For the general public though, BMI is reasonable computation to determine where you stand. You can calculate your BMI here.
There’s no shortage of research and debate over which types of diet and exercise are most beneficial for sustainable weight loss. It’s well-known obesity is a strong risk factor hyperlipidemia, type 2 diabetes, cardiovascular disease and certain cancers (b). Despite health authorities, doctors and government recommendations for low-fat and low-calorie diets, the obesity epidemic continues to spiral out of control. It’s estimated over a third of the world population is overweight or obese (c). By 2030, if secular trends continue, the direst projections show 86.3% of the USA adult population will fall into this category, and the prevalence of overweight children will double, with associated health-care costs ranging from $860.7-956.9 billion (d).
So, what can we do to reverse this scary forecast? Keto! If you’re like millions of Americans who have tried a low-calorie, low-fat diet but didn’t get lasting results or felt miserable in the process, it’s time to consider a new approach supported by your physiology and evidence-based studies. There is solid research showing low calorie diets are ineffective for permanent weight loss (e). Changing long-held dietary beliefs is always controversial and initially resisted, but there are dozens of high-quality studies showing more weight loss with low-carb diets compared to other modalities. For example, a Meta-Analysis reviewed randomized controlled trials comparing the effects of low-carb vs low-fat diets on weight and cardiovascular disease (CVD) risk. While both groups had weight loss and improvement in CVD risk factors, the low-carb group had greater improvements in both areas (f). Alsimportant to consider is the weight being loss is actually fat and not lean body mass. No one wants to lose what the muscle they’ve worked for in the gym! Studies have shown a very low carbohydrate diet (<50g or 10% of calories from carbohydrate) reduced body fat but not total body weight, suggesting lean mass is preserved or increased (g).
It’s true, most commercial and conventional diets will result in temporary weight loss but finding sustainable solutions to prevent weight regain is another beast. One of the best ways to change your body’s set-point weight in the hypothalamus (“link to set-point weight”) is by lowering your insulin levels through a low-carbohydrate, ketogenic diet. Failing to address hyperinsulinemia and accounting for the physiological compensatory mechanisms behind low calorie diets are largely why they fail long-term. We know keto, sometimes combined with intermittent fasting, nips hyperinsulinemia by reducing the need for insulin due to low carbohydrate consumption.
b) Hurby A and Hu FB. The Epidemiology of Obesity: A Big Picture. Pharmacoeconomics. 2015 Jul; 33(7):673-689 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4859313/
c) Wang Y, Beydoun MA, Liang L, Cballero B, Kumanyika SK. Will all Americans become overweight or obese? Estimating the progression and cost of the US obesity epidemic. Obesity (Silver Spring). 2008. Oct:16(10):2323-30. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4859313/#R5
d) Paoli, A. Ketogenic Diet for Obesity: Friend or Foe? Int J Environ Res Public Health. 2014 Feb; 11(2):2092 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945587/
e) Tomiyama AJ, Mann T, Vinas D, Hunger JM, DeJager J, Taylor SE. Low Calorie Dieting Increases Cortisol. Psychosom Med. 2010 May; 72(4): 357-364 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2895000/
f) Sackner-Bernstein J, Kanter D, Kaul S. Dietary Intervention for Overweight and Obese Adults: Comparison of Low-Carbohydrate and Low Fat Diets: A Meta-Analysis. PLoS One. 2015 Oct 20;10(10). https://www.ncbi.nlm.nih.gov/pubmed/2648570
g) Hashimoto Y, Fukuda T, Oyabu C, Tanaka M, Asano M, Yamazaki M, Fukui M. Impact of a low carbohydrate diet on body composition: meta-analysis of randomized controlled studies. Obes Rev. 2016 Jun 17 (6):499-509 https://www.ncbi.nlm.nih.gov/pubmed/27059106
2. Type 2 Diabetes: The most common form of Diabetes Mellitus, is type 2 (T2DM), often referred to as adult-onset. Unfortunately, due to the standard American diet (SAD), we’re seeing it develop in younger and younger patients, even teenagers. Years of eating crappy processed junk food with vegetable oils, sugars, and low nutritional value creates a state of hyperinsulinemia and insulin resulting in chronically elevated blood glucose levels (hyperglycemia). Without intervention, chronic hyperglycemia will become pre-diabetes then diabetes. Despite the plethora of medications on the market today, there still isn’t a pharmacological cure. Some examples of current treatment options include biguanides (Metformin), sulfonylureas (Glipizide, Glyburide), thiazolidinediones (Actos, Avandia), alpha glucosidase inhibitors (Precose), meglitinides (Prandin, Starlix), amylin analogues (Symlin), sodium glucose co-transporter 2 inhibitors (Jardiance, Invokana), glucagon-like peptide-1 receptor agonists (Victoza, Ozempic), dipeptidyl peptidase-4 inhibitors (Januvia, Onglyza) and insulin (Lispro, Humalog, Glargine, Aspart). These medications work in different ways and have varying side-effects, some including weight gain and increased risk of microbial infections (h).
The good news is, you may not need your medications forever! Fortunately we have studies to show diet alone can be an effective way to put T2DM into remission without any injections or daily pills (I,j,k,l). A low-carbohydrate, high fat, moderate protein ketogenic diet reduces the need for your pancreas to produce high amounts of insulin to tame elevated blood sugar. Dietary fat doesn’t stimulate insulin the way carbohydrates do, or even proteins. By adhering to keto, patients can effectively reverse insulin resistance and normalize their blood sugars without medications, or at least decrease the dosage over time. Safely weaning off of insulin is a huge win for overall health and wellness! Before starting Keto, diabetic patients need to consult with their primary doctor and make him or her aware of your new eating habits as blood sugar can drop rapidly causing hypoglycemia. Close monitoring of your sugar level and medication adjustments are needed and must be done in conjunction with your personal doctor.
h) Steinberg J and Carlson L. Type 2 Diabetes Therapies: A STEPS Approach. Am Fam Physician. 2019 Feb 15;99 (4): 237-243.
i) Sainsbury E, Kizirian NV, Partridge SR, Gill T, Colagiuri S, Gibson AA. Effect of dietary carbohydrate restriction on glycemic control in adults with diabetes: A systemic review and meta-analysis. Diabetes Res Clin Prat. 2018 May; 139:239-252. https://www.ncbi.nlm.nih.gov/pubmed/29522789
j) Wang LL, Wang Q, Hong Y, Ojo O, Jiang Q, Hou YY, Huang YH, Wang XH. The Effect of Low-Carbohydrate Diet on Glycemic Control in Patients with Type 2 Diabetes Mellitus. Nutrients. 2018 May 23;10(6). https://www.ncbi.nlm.nih.gov/pubmed/29882884
k) Saslow LR, Daubenmier JJ, Moskowitz JT, Kim S, Murphy EJ, Phinney SD, Ploutz-Snyder R, Goldman V, Cox RM, Mason AE, Moran P, Hecht FM. Twelve-month outcomes of a randomized trial of moderate-carbohydrate versus very low-carbohydrate diet in overweight adults with type 2 diabetes mellitus or prediabetes. Nutrition & Diabetes 7, Article number: 304(2017). https://www.nature.com/articles/s41387-017-0006-9
l) Westman EC, Tondt J, Maguire E, Yancy WS Jr. Implementing a low-carbohydrate, ketogenic diet to manage type 2 diabetes mellitus. Exper Rev Endocrinol Metab. 2018 Sep; 13(5):263-272.
3. Epilepsy: Watching somebody experience a seizure can leave you feeling helpless and frightened. If you suffer from seizures, you know the implications last beyond the episode. Abnormal activity in the brain can provoke seizures ranging from temporary confusion, blank stares, uncontrollable jerking movements of the limbs or loss of consciousness. Epilepsy is a spectrum seizure disorder and the 4th most common neurological disorder, affecting people of all ages and race (m). Dysfunction or dysregulation of neurotransmitters in the brain, such as glutamate (excitatory) and GABA (inhibitory) cause neurons to fire when they aren’t supposed to, altering the electrical activity in the brain, resulting in seizures.
In the 1920s, before many pharmacological treatments for seizures arrived on the scene, the ketogenic diet was used with great success to reduce frequency of seizure activity in pediatric epileptic patients (n). Over the past few decades, supplying the brain with ketones has resulted in improvement for seizure disorders as well as other neurological illnesses in children and adults alike (o). By some estimates, the ketogenic diet can reduce seizure frequency by 50% or more (p) from reduction of glutamate while also increasing synthesis of GABA. This is in addition to the systemic anti-inflammatory effects the keto diet produces. There have also been emerging studies on alteration in the gut microbiome from a keto diet causing changes in the proportion of GABA to Glutamate (q). We are just beginning to discover the many applications of a ketogenic diet for neurological disease but it’s role in epilepsy is well established.
o) Baranano KW, Hartman AL. The Ketogenic Diet: Uses in Epilepsy and Other Neurological Illnesses. Curr Treat Options Neurol. 2008 Nov; 10(6) 410-419. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898565/
p) Williams TJ, Cervenka MC. The role for ketogenic diets in epilepsy and status epilepticus in adults. Clin Neurophysiol Pract. 2017; 2:154-160. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6123874/
4. Polycystic Ovarian Syndrome (PCOS): Women of reproductive age can be devastated by this hormonal disorder. Signs and symptoms range in severity but include follicles or cysts in the ovaries, irregular or prolonged periods, and elevated levels of androgens (male hormones) causing excess body and facial hair along with acne and male-pattern baldness. Unfortunately, PCOS can lead to infertility, gestational diabetes, fatty liver disease, metabolic syndrome, type 2 diabetes, depression, anxiety, and endometrial cancer (r). There is a strong association of obesity with some estimates being up to 80% of overweight and obese women having PCOS (s).
The exact cause of PCOS is still unclear but we know there’s a substantial connection to excess weight, insulin resistance and metabolic syndrome (t,u). So, it would be intuitive to make dietary changes to naturally restore insulin sensitivity and reverse metabolic syndrome while reducing weight. A healthy keto diet can accomplish all of this! More and more promising studies are demonstrating the success of a low-carbohydrate diet on PCOS and fertility (v,w,x,y).
s) Sam S. Obesity and Polycystic Ovary Syndrome. Obes Manag. 2007 Apr; 3(2):69-73. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2861983/
t) Moini A, Javanmard F, Eslami B, Aletaha N. Prevalence of metabolic syndrome in polycystic ovarian syndrome women in a hospital of Tehran. Iran J Reprod Med. 2012 Mar; 10(2): 127-130. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163274/
u) Mandrelle K, Kamath MS, Bondu DJ, Chandy A, Aleyamma TK, George K. Prevalence of metabolic syndrome in women with polycystic ovary syndrome attending an infertility clinic in a tertiary care hospital in south India. J Hum Reprod Sci. 2012 Jan-Apr; 5(1):26-31. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3409916/
v) McGrice M and Porter J. The Effect of Low Carbohydrate Diets on Fertility Hormones and Outcomes in Overweight and Obese Women: A Systemic Review. Nutrients. 2017, 9(3), 204. https://www.mdpi.com/2072-6643/9/3/204/htm
w) Gower BA, Chandler-Laney PC, Ovalle F, Goree LL, Azziz R, Desmond RA, Granger WM, Goss AM, Bate GW. Favourable metabolic effects of a eucaloric lower-carbohydrate diet in women with PCOS. Clin Endocrinol (Oxf). 2013 Oct;79(4):550-7. https://www.ncbi.nlm.nih.gov/pubmed/23444983
x) Phy JL, Pohlmeier AM, Cooper JA, Watkins P, Spallholz J, Harris KS, Berenson AB, Boylan M. Low Starch/Low Dairy Diet Results in Successful Treatment of Obesity and Co-Morbidities Linked to Polycystic Ovary Syndrome (PCOS). J Obes Weight Loss Ther. 2015 Apr; 5(2):259. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4516387/
y) Douglas CC, Gower BA, Darnell BE, Ovalle F, Oster RA, Azziz R. Role of diet in the treatment of polycystic ovary syndrome. Fertil Steril. 2006 Mar: 85(3): 679-688. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3752890/
5. Migraines: If you’ve dealt with one these harrowing headaches knows how debilitating they can be. Migraines can last for days without abating and often recur frequently. Migraines have varying presentations but commonly start on one side of the head (unilateral) with a throbbing ache and are accompanied by nausea, vomiting, sensitivity to light (photophobia) and sensitivity to sound (phonophobia). Some people develop terrifying auras before or during migraines involving loss of vision, weakness or numbness in parts of the face or body, difficulty speaking, and visual disturbances. It’s not uncommon for 1st time migraine sufferers to show up in the ER thinking they’ve had a stroke. Even after a migraine has subsided brain fog, confusion, dizziness, malaise and light sensitivity can last for an additional day or two. Not cool when you’re trying to be a functional member of society.
The physiological cause of migraines isn’t fully understood yet. Theories have evolved from changes in brain’s blood flow and vasculature to also include altered levels of serotonin (z) and estrogen influence (aa). Abortive migraine medications are classified as ‘triptans and work by activating serotonin receptors in the brain to increase serotonin levels and produce a vaso-constrictive response. There are also theories about excitatory neurotransmitter glutamate’s role in migraines (bb,cc). The exact mechanism behind Keto improving migraines is still being worked out, and it’s possibly due to the anti-inflammatory effect with ketones reducing glutamate-induced free radicals (dd).
Seizure medication, Topiramate (Topamax), has recently been used as a preventative treatment option for migraine patients. The side-effects of nausea, paresthesias, hair loss (alopecia), and depression can be just as upsetting as the headaches themselves. Topiramate functions to antagonize glutamate receptors and augment GABA (inhibitory neurotransmitter) activity which may explain why it can reduce migraine frequency in some patients.
As we discussed above, the keto diet has been a wonderful treatment option for seizures amongst other neurological disorders, so it makes sense for the keto diet to help reduce another neurological disorder: migraines. If seizure medications can be used as part of migraine pharmacotherapy, then perhaps a diet proven to benefit epilepsy will also benefit migraines. Of course, we have promising studies to back this up and prompt further evaluation to better understand the mechanism (ee,ff,gg).
z) Hamel E. Serotonin and migraine: biology and clinical implications. Cephalalgia. 2007 Nov;27(11):1293-300. https://www.ncbi.nlm.nih.gov/pubmed/17970989
aa) Aggarwal M, Puri V, Puri S. Serotonin and CGRP in Migraine. Ann Neurosci. 2012 Apr; 19(2): 88-94. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4117050/
bb) Vikelis M, Mitsikostas DD. The role of glutamate and its receptors in migraine. CNS Neurol Disord Drug Targets. 2007 Aug;6(4):251-7. https://www.ncbi.nlm.nih.gov/pubmed/17691981
cc) D’Andrea Giovanni. Granella F, Cataldini M, Verdelli F, Balbi T. GABA and glutamate in migraine. J Headache Pain. 2001 Sep; 2(Suppl 1): s57-s60 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3451832/
dd) Maalouf M, Sullivan PG, Davis L, Young Kim D, Rho JM. Neuroscience. 2007 Mar 2; 145(1):256-264. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1865572/
ee) Di Lorenzo C, Coppola G, Sirianni G, Pierelli F. Short term improvement of migraine headaches during ketogenic diet: a prospective observational study in a dietician clinical setting. J Headache Pain. 2013; 14 (Suppl 1): P219. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3620251/
ff) Barbanti P, Fofi L, Aurilia C, Egeo G, Caprio M. Ketogenic diet in migraine: rationale, findings and perspectives. Neurol Ci. 2017 May;38(Suppl 1): 111-115. https://www.ncbi.nlm.nih.gov/pubmed/28527061
gg) Gross EC, Klement RJ, Schoenen J, D’Agostino DP, Fischer D. Potential Protective Mechanism of Ketone Bodies in Migraine Prevention. Nutrients. 2019 Apr 10;11(4). https://www.ncbi.nlm.nih.gov/pubmed/30974836