When a low carbohydrate diet is started, weight loss usually occurs rapidly and easily. Although the initial loss is partly water weight, with consistency, body-fat loss continues until ideal body weight is reached. This usually happens without much discomfort.
There are occasionally exceptions to this experience. I previously recommended staying well hydrated, not being afraid to eat fat, and adding a little extra salt to improve the transition to a low carbohydrate diet. Metabolically, your body is designed to switch over to fat burning when carbohydrates are restricted, and this transition occurs over a matter of weeks.
But some people have a difficult time sticking to this plan. Hunger doesn't always diminish. Eventually willpower is exhausted. What is going on?
This happens most often in people that have struggled with weight for a long time. This could be long-standing obesity or yo-yo dieting.
INSULIN CAUSES OBESITY
I previously discussed the importance of insulin in weight loss/gain. Gary Taubes in "Why We Get Fat And What To Do About It," makes a very well supported argument that elevated insulin causes us to gain weight, and makes it difficult to reduce weight, even with calorie restriction. Recall that carbohydrates are the primary driver of insulin. A low carbohydrate diet reduces insulin levels and thus allows weight loss.
Jason Fung in "The Obesity Code" discusses the importance of insulin resistance. This is a common problem and often underlies difficulty with weight loss.
Our bodies maintain homeostasis. That means they adjust to the situation to maintain consistency. Let's see how this works with insulin. When a person eats a meal containing carbohydrates, their blood glucose level will rise. To maintain homeostasis (consistent blood glucose level) the pancreas secretes insulin. This elevated insulin level drives the blood glucose into cells to be burned as energy or stored as fat. It simultaneously stops mobilizing fat from storage since energy is plentiful. This is all good.
Now let's assume the person eats a high carbohydrate diet consistently, just as recommended by the government. The insulin level is elevated throughout the day. Because insulin drives glucose into cells, the blood sugar level drops and appetite increases. So they reach for a snack. Usually this is a high carbohydrate snack or beverage. This again raises insulin. Some have recommended "grazing." This means eating many small meals throughout the day. Obviously this will maintain a steady flow of carbohydrates into the bloodstream, with the resulting elevation in insulin level.
As an aside - It is highly doubtful that our ancestors evolved during times when high-carbohydrate foods were available at all times. In fact it is doubtful that hunter-gatherers had constant access to ANY foods. So the idea that eating all the time (even when driving) makes any sense is ridiculous.
Anyway, because elevated insulin causes weight gain, the person gains weight. Homeostasis applies to cells specifically, just as it does to the body in general. What does this mean? As fat cells get increasingly full of stored fat they become increasingly resistant to additional storage. Because insulin is the hormone telling them to store more fat they become insulin resistant. This happens throughout our body. The body responds by further increasing the insulin secretion until blood sugar drops into the desired range. This cycle continues over and over. Insulin resistance worsens over time. The ever higher insulin level prevents mobilization of body fat for energy and increases appetite, intensifying the problem.
THIS CYCLE MUST BE BROKEN TO ACHIEVE WEIGHT LOSS.
Carbohydrates are the most powerful driver of insulin. Protein also causes insulin release, but significantly less than carbohydrates. Dietary fat causes minimal insulin release. Usually, insulin resistance improves dramatically when carbohydrates are restricted.
If you struggle with a low carbohydrate diet, if you feel hungry all the time in spite of eating dietary fat, if weight loss stalls, you very likely have significant insulin resistance.
WHAT TO DO?
1- Make sure you are really not eating carbohydrates. They are snuck into everything- especially processed foods and in restaurants. Read labels. Even better- make your own food. Stick with non-starchy vegetables and meats and dietary fat.
2- Don't eat tons of protein.
3- Avoid artificial sweeteners. Although they contain minimal to no calories, studies have shown they cause insulin release. That diet soda will actually make you fat. Avoiding sweet tasting foods will gradually reduce their desirability.
4- The most powerful way to break through insulin resistance is with fasting. Our pancreas secretes insulin as we prepare to take a bite of food. Additional insulin is released during chewing and swallowing in anticipation of the subsequent blood sugar elevation. Therefore, completely avoiding food will minimize insulin levels. Back to homeostasis. As our blood insulin level drops, our cells release stored body fat for energy. As we maintain a low insulin level by extending the fast, our cells will become more sensitive to insulin again. This can actually reverse insulin resistance. Although fasting initially sounds crazy, it turns out to be fairly easy.
I have consistently maintained a low carbohydrate diet now for over two-and-a-half years. I have never felt better. As I discussed previously, I find this way of eating very sustainable because my body functions better than ever.
Anyway, I have gotten accustomed to the lack of cravings associated with this diet. So much so, that I was surprised the other night when I returned home after a evening out with friends. We had eaten dinner at a local restaurant. The pureed squash soup and the pork chop I ordered were delicious, and the portions were generous. I remember briefly thinking that both were a bit sweeter than I had expected, but it was not until later that I realized just how much sugar they had contained. As usual, we bypassed dessert and left the restaurant pleasantly satisfied.
By the time we returned home from our evening out (only a couple of hours after eating a substantial dinner) I was ravenously hungry again. This was particularly startling to me, because since I have adopted a low carbohydrate diet, I rarely feel the need to snack, and I never have this level of aggressive hunger.
I ate a handful of almonds with some 85% cacao and drank a glass of water. This settled things down a bit and I resumed my normal diet in the morning with bacon and eggs.
So what happened here?
I inadvertently consumed much more sugar than I am accustomed to at dinner that night. This caused my blood sugar to elevate. My body released a large bolus of insulin in response. This dropped my blood sugar, which aggressively activated my hunger. The trap would have been to eat another carbohydrate rich meal causing this cycle to repeat.
This cycle of carbohydrate overconsumption, leading to increased insulin secretion, leading to hunger, leading to carbohydrate overconsumption is essentially the standard American diet. This causes many Americans to be chronically hungry even though they are overweight.
This cycle can only be broken by reducing carbohydrate intake. Insulin secretion and hunger are involuntary. Carbohydrate consumption is a choice. Choosing to reduce carbohydrate intake reduces your bodies need to secrete insulin and thus reduces hunger. This results in weight loss.
The evening I described was notable since is is now rare for me. I used to feel this way all the time. The foods we eat are more than just calories, vitamins and minerals. They also influence how our bodies function via their hormonal effects. Dietary recommendations that ignore the hormonal response to macronutrients are far too simplistic.
I previously suggested that we should not fear dietary fat. It appears that dietary fat of all types has gotten a bad rap, especially saturated fat. People are sometimes reluctant to increase dietary fat however, because they have heard for decades that "fat was bad," and that they should eat a high-carbohydrate diet for health. I believe the science is gradually correcting itself, and the case against fat is being challenged throughout the world.
Occasionally, I will be discussing nutrition with someone and they proudly tell me how they have gotten over their fear of eating fat. I have lost track of how many times I have heard, "I'm drinking bulletproof coffee!" but then they question why their hunger has not decreased, and they have not lost any weight.
At this point I ask them to take me through a typical day of eating. I am often surprised to hear that while they have increased their dietary fat intake, they have not also reduced their carbohydrate intake. It seems the "healthiness" of whole grains has been imprinted into our minds.
I do not believe you will achieve health benefits from adding dietary fat to a high-carbohydrate diet. In fact, this will likely be counter-productive.
Our goal needs to be reducing our bodies production of insulin. This occurs when carbohydrate intake is reduced. Dietary fat causes minimal to no insulin stimulation, and thus substituting fat for carbohydrates is the goal. We should not be simply adding fat to a high-carbohydrate diet. The most important part of the diet I advocate, and follow myself, is reducing carbohdrates.
When following a properly formulated low-carbohydrate, high-fat diet your hunger will naturally decrease, cravings will subside, and it becomes easy to skip meals. If you attempt this kind of dietary change, and within a few days or weeks you have not noticed these changes, please carefully evaluate your food choices and make sure you are truly eating low carb.
Some foods commonly felt to be healthy but contain high levels of carbohydrates include oatmeal, whole grain bread and beans. These foods must be skipped if your goal is to reduce carbohydrate intake.
If there are foods you are unsure of, please ask me about them in the comment section below and I will be happy to reply with my recommendations.
Soon after beginning to eat a low-carbohydrate, high-fat diet I found myself eating because it was "time to eat" not necessarily because I was hungry. Without doing much research at the time, I decided to skip a meal and see what happened. Amazingly, I found that when I skipped lunch I made it all the way to dinner. I did not instantly lose all my muscle mass, nor did I experience lack of energy. Then I skipped breakfast and lunch. This felt strange to me as it was contrary to the often recited recommendation to eat many small meals throughout the day. I had repeatedly heard that skipping breakfast increases the likelihood of developing obesity and diabetes. Loss of lean muscle mass was also commonly cited. It seemed like I was embarking on exactly the wrong path.
And yet it made no sense to me to eat when I was not hungry. Especially when I felt better during the fasted state. It seemed to me I had stumbled upon yet another myth of modern nutrition- that humans need to be eating constantly. Thinking back to a time before industrial food and agriculture companies, our ancestors were hunter gatherers and probably experienced widely varying caloric intakes over time. Perhaps intermittent fasting was actually the normal situation back then. Individuals that thrived under such conditions would have been more likely to pass on their genes to future generations. In the modern day, with abundant low nutrient density foods omnipresent, those genes that led to survival back then may have become counterproductive. Perhaps if we mimic ancestral conditions by varying food intake as opposed to continually flooding our bodies with food we also will thrive.
There have been many studies on this topic and most show intermittent fasting is likely to be quite good for us. Let's look at some of the major findings:
The concept of the yo-yo diet is well known. Diets, in the traditional sense are temporary, unpleasant restrictions in food quantity that result in some amount of weight loss. Once the diet ends, most people regain all the weight they lost and usually a little bit more. Over time they end up gaining weight. This is not metabolically healthy. Studies investigating intermittent fasting have shown reductions in both body weight and body fat while maintaining or even adding lean body mass.
Additionally, people tend to find intermittent fasting much more sustainable than simple caloric restriction. This is probably because intermittent fasting may induce a temporary state of nutritional ketosis, especially when done as part of a low-carbohydrate, high-fat diet. Ketosis fuels your body with fat metabolites (ketone bodies) and thus suppresses hunger and provides abundant energy during the fast.
Studies consistently show improved insulin sensitivity as a result of intermittent fasting protocols. Remember our discussion of increased baseline insulin secretion that results from exposure to a high-carbohydrate diet? Intermittent fasting reverses this. When not exposed to carbohydrates and proteins for a period of time, the pancreas is able to reduce insulin production and our cells then are exposed to lower insulin levels. The cells in turn will up-regulate their insulin receptors. And just like that, insulin sensitivity improves. It makes sense and studies confirm this.
Heart attack animal models have shown less heart muscle damage after myocardial infarction (heart attack) if the animal was on an intermittent fasting protocol. Additionally, lipid profiles improve with intermittent fasting. Increased HDL(good cholesterol), decreased triglycerides and decreased total cholesterol were seen in multiple studies. Reduction in systolic and diastolic blood pressure that results from intermittent fasting places a decreased load on the heart. Lastly, intermittent fasting resulted in markedly improved survival in a congestive heart failure animal model. It should be noted that lipid profiles do not necessarily improve in patients with familial hypercholesterolemia, and this technique should probably be avoided in this unique situation.
Intermittent fasting has been found to reduce neuron damage in animal stroke models, reduce spinal cord demyelination in multiple sclerosis animal models, prevent age-related impairment of brain function, increase neuronal resistance to injury, and may even protect neurons against the degenerative changes that cause Alzheimer's dementia.
Patients commonly report feeling reduced anxiety and improved ability to focus during a fast. Studies report reduced impulsivity, decreased anger, decreased confusion and improved vigor while on an intermittent fasting protocol.
Immune System Support
Mice adapted to intermittent fasting showed an improved immune response to, and faster clearance of a Salmonella infection compared to those allowed to eat freely.
Since we have been discussing a variety of protective effects associated with intermittent fasting, it comes as no surprise to hear that intermittent fasting is associated with reduced inflammatory markers in blood tests.
Caloric restriction and ketogenic diets have been show to be effective against some cancers in animal models. Dormant cancer cells are dependent on anaerobic glucose metabolism. These cells can result in cancer relapses. Since blood glucose levels can be decreased by up to 40% during fasting, it is felt that fasting may cause these dormant cells to die. Early prostate cancer animal studies show a trend toward improved survival in the intermittent fasting group.
Mice that had adapted to intermittent fasting suffered less damage when exposed to gamma radiation. This protective effect was lost when the mice were allowed to eat freely.
In addition to the potential health benefits, there are some more immediate, practical benefits of intermittent fasting as well:
It is free. I recommend consuming grass-fed, grass-finished meats, wild caught fish, and organic vegetables whenever possible. These foods are more expensive than the standard versions. Skipping meals helps to offset this expense.
It is fast. You will not have to spend any time preparing breakfast or lunch on fasting days.
Improved productivity. The lunch hour is now free-time during which other things can be done.
How to do it?
1- Train your body to burn body fat for energy. This will greatly facilitate transitioning into intermittent fasting. In my case it happened automatically. Read my earlier blog postings for details. Start with carbohydrate restriction, make sure you are eating the proper amount of protein, and don't be afraid to eat fat. You must eat fat to burn fat.
2- Your body will adapt to preferentially burning fat over a period of weeks. During the first two weeks you may feel a bit strange, you will likely lose 10 or more pounds. Stay well hydrated and eat healthy fats when hungry.
3- Within 6 weeks of beginning a low carbohydrate diet many people easily and automatically transition into intermittent fasting. If you would like to try this - simply skip breakfast and lunch and eat a proper dinner. Stay well hydrated throughout the day. Black coffee and tea can be consumed during the fast. To sleep properly, stop consuming caffeine by 2PM. Water should be consumed throughout the day.
4- It appears the beneficial effects of fasting require at least 12 hours without eating, and benefits increase with longer fasting periods. Although fasting can safely be extended beyond 24 hours, most people do not need to. Because eating is also a social event, I prefer fasting from after dinner until dinner the next day. This way I can sit down and enjoy eating with my family, and it provides me an easily sustainable 18-20 hour fasting period. Sleeping through a large portion of this fasting period makes this even easier.
5- Bulletproof coffee. This is a "biohack" developed by Dave Asprey. Adding some butter and coconut oil or MCT oil to black coffee and then blending, it creates tiny droplets of fat suspended in the coffee. Try a teaspoon of each to start and adjust as needed. At first this might seem like it would be unpalatable, but I encourage you to try it with an open mind. It not only tastes much better than expected, it has an excellent mouth feel, and makes you feel good. It helps your body to produce ketone bodies (especially if MCT oil is used). It takes advantage of how our body metabolizes dietary fat. When we consume pure fat while in a fasted state, our body will continue to function as if it is fasting. There is no insulin response. Dave Asprey markets a more refined version of MCT oil he calls Brain Octane Oil. It includes only the 8 chain fatty acids which produce ketone bodies most efficiently. I started intermittent fasting initially drinking bulletproof coffee for breakfast and lunch. I gradually transitioned back to black coffee as my body adjusted and seemed to mobilize stored energy better.
6- When breaking the fast, do not calorie restrict. Eat a proper meal at a proper pace. A large salad, some high quality meat or fish and a small serving of white rice or sweet potato. Fill your plate and enjoy your meal.
Wahl D, Cogger VC, Solon-Biet SM, Waern RV, Gokarn R, Pulpitel T, Cabo Rd, Mattson MP, Raubenheimer D, Simpson SJ, Le Couteur DG. Nutritional strategies to optimise cognitive function in the aging brain. Ageing Res Rev. 2016 Nov;31:80-92. doi: 10.1016/j.arr.2016.06.006. Epub 2016 Jun 26. Review. PubMed PMID: 27355990; PubMed Central PMCID: PMC5035589.
Dashti HS, Mogensen KM. Recommending Small, Frequent Meals in the Clinical Care of Adults: A Review of the Evidence and Important Considerations. Nutr Clin Pract. 2016 Sep 1. pii: 0884533616662995. [Epub ahead of print] Review. PubMed PMID: 27589258.
Tinsley GM, Forsse JS, Butler NK, Paoli A, Bane AA, La Bounty PM, Morgan GB, Grandjean PW. Time-restricted feeding in young men performing resistance training: A randomized controlled trial. Eur J Sport Sci. 2016 Aug 22:1-8. [Epub ahead of print] PubMed PMID: 27550719.
Jarvie BC, King CM, Hughes AR, Dicken MS, Dennison CS, Hentges ST. Caloric restriction selectively reduces the GABAergic phenotype of mouse hypothalamic proopiomelanocortin neurons. J Physiol. 2016 Aug 17. doi: 10.1113/JP273020. [Epub ahead of print] PubMed PMID: 27531218.
Gow ML, Garnett SP, Baur LA, Lister NB. The Effectiveness of Different Diet Strategies to Reduce Type 2 Diabetes Risk in Youth.Nutrients. 2016 Aug 9;8(8). pii: E486. doi: 10.3390/nu8080486. Review. PubMed PMID: 27517953; PubMed Central PMCID: PMC4997399.
Arciero PJ, Edmonds R, He F, Ward E, Gumpricht E, Mohr A, Ormsbee MJ, Astrup A. Protein-Pacing Caloric-Restriction Enhances Body Composition Similarly in Obese Men and Women during Weight Loss and Sustains Efficacy during Long-Term Weight Maintenance. Nutrients. 2016 Jul 30;8(8). pii: E476. doi: 10.3390/nu8080476. PubMed PMID: 27483317; PubMed Central PMCID: PMC4997389.
Varady KA. Impact of intermittent fasting on glucose homeostasis. Curr Opin Clin Nutr Metab Care. 2016 Jul;19(4):300-2. doi: 10.1097/MCO.0000000000000291. PubMed PMID: 27137896.
Harvie MN, Howell T. Could Intermittent Energy Restriction and Intermittent Fasting Reduce Rates of Cancer in Obese, Overweight, and Normal-Weight Subjects? A Summary of Evidence. Adv Nutr. 2016 Jul 15;7(4):690-705. doi: 10.3945/an.115.011767. Print 2016 Jul. Review. PubMed PMID: 27422504; PubMed Central PMCID: PMC4942870.
Longo VD, Panda S. Fasting, Circadian Rhythms, and Time-Restricted Feeding in Healthy Lifespan. Cell Metab. 2016 Jun 14;23(6):1048-59. doi: 10.1016/j.cmet.2016.06.001. Review. PubMed PMID: 27304506.
Joslin PM, Bell RK, Swoap SJ. Obese mice on a high-fat alternate-day fasting regimen lose weight and improve glucose tolerance.J Anim Physiol Anim Nutr (Berl). 2016 Jun 8. doi: 10.1111/jpn.12546. [Epub ahead of print] PubMed PMID: 27273295.
Belaïch R, Boujraf S, Benzagmout M, Magoul R, Maaroufi M, Tizniti S. Implications of oxidative stress in the brain plasticity originated by fasting: a BOLD-fMRI study. Nutr Neurosci. 2016 Jun 8:1-8. [Epub ahead of print] PubMed PMID: 27276372.
Razeghi Jahromi S, Ghaemi A, Alizadeh A, Sabetghadam F, Moradi Tabriz H, Togha M. Effects of Intermittent Fasting on Experimental Autoimune Encephalomyelitis in C57BL/6 Mice. Iran J Allergy Asthma Immunol. 2016 Jun;15(3):212-9. PubMed PMID: 27424136.
Nair PM, Khawale PG. Role of therapeutic fasting in women's health: An overview. J Midlife Health. 2016 Apr-Jun;7(2):61-4. doi: 10.4103/0976-7800.185325. Review. PubMed PMID: 27499591; PubMed Central PMCID: PMC4960941.
Hou L, Wang D, Chen D, Liu Y, Zhang Y, Cheng H, Xu C, Sun N, McDermott J, Mair WB, Han JD. A Systems Approach to Reverse Engineer Lifespan Extension by Dietary Restriction. Cell Metab. 2016 Mar 8;23(3):529-40. doi: 10.1016/j.cmet.2016.02.002. PubMed PMID: 26959186.
Sibille KT, Bartsch F, Reddy D, Fillingim RB, Keil A. Increasing Neuroplasticity to Bolster Chronic Pain Treatment: A Role for Intermittent Fasting and Glucose Administration? J Pain. 2016 Mar;17(3):275-81. doi: 10.1016/j.jpain.2015.11.002. Epub 2016 Feb 2. PubMed PMID: 26848123; PubMed Central PMCID: PMC4824292.
Chamari K, Briki W, Farooq A, Patrick T, Belfekih T, Herrera CP. Impact of Ramadan intermittent fasting on cognitive function in trained cyclists: a pilot study. Biol Sport. 2016 Mar;33(1):49-56. doi: 10.5604/20831862.1185888. Epub 2015 Dec 30. PubMed PMID: 26985134; PubMed Central PMCID: PMC4786586.
Gotthardt JD, Verpeut JL, Yeomans BL, Yang JA, Yasrebi A, Roepke TA, Bello NT. Intermittent Fasting Promotes Fat Loss With Lean Mass Retention, Increased Hypothalamic Norepinephrine Content, and Increased Neuropeptide Y Gene Expression in Diet-Induced Obese Male Mice. Endocrinology. 2016 Feb;157(2):679-91. doi: 10.1210/en.2015-1622. Epub 2015 Dec 14. PubMed PMID: 26653760; PubMed Central PMCID: PMC4733124.
Campos-Rodríguez R, Godínez-Victoria M, Reyna-Garfias H, Arciniega-Martínez IM, Reséndiz-Albor AA, Abarca-Rojano E, Cruz-Hernández TR, Drago-Serrano ME. Intermittent fasting favored the resolution of Salmonella typhimurium infection in middle-aged BALB/c mice. Age (Dordr). 2016 Feb;38(1):13. doi: 10.1007/s11357-016-9876-3. Epub 2016 Jan 21. PubMed PMID: 26798034; PubMed Central PMCID: PMC5005893.
Cherif A, Roelands B, Meeusen R, Chamari K. Effects of Intermittent Fasting, Caloric Restriction, and Ramadan Intermittent Fasting on Cognitive Performance at Rest and During Exercise in Adults. Sports Med. 2016 Jan;46(1):35-47. doi: 10.1007/s40279-015-0408-6. Review. PubMed PMID: 26438184.
Seimon RV, Shi YC, Slack K, Lee K, Fernando HA, Nguyen AD, Zhang L, Lin S, Enriquez RF, Lau J, Herzog H, Sainsbury A. Intermittent Moderate Energy Restriction Improves Weight Loss Efficiency in Diet-Induced Obese Mice. PLoS One. 2016 Jan 19;11(1):e0145157. doi: 10.1371/journal.pone.0145157. eCollection 2016. PubMed PMID: 26784324; PubMed Central PMCID: PMC4718562.
BaHammam AS, Pandi-Perumal SR, Alzoghaibi MA. The effect of Ramadan intermittent fasting on lipid peroxidation in healthy young men while controlling for diet and sleep: A pilot study. Ann Thorac Med. 2016 Jan-Mar;11(1):43-8. doi: 10.4103/1817-1737.172296. PubMed PMID: 26933456; PubMed Central PMCID: PMC4748614.
Zarrouk N, Hammouda O, Latiri I, Adala H, Bouhlel E, Rebai H, Dogui M. Ramadan fasting does not adversely affect neuromuscular performances and reaction times in trained karate athletes. J Int Soc Sports Nutr. 2016 Apr 19;13:18. doi: 10.1186/s12970-016-0130-2. eCollection 2016. PubMed PMID: 27099568; PubMed Central PMCID: PMC4837563.
Zuo L, He F, Tinsley GM, Pannell BK, Ward E, Arciero PJ. Comparison of High-Protein, Intermittent Fasting Low-Calorie Diet and Heart Healthy Diet for Vascular Health of the Obese. Front Physiol. 2016 Aug 29;7:350. doi: 10.3389/fphys.2016.00350. eCollection 2016. PubMed PMID: 27621707; PubMed Central PMCID: PMC5002412.
Singh R, Manchanda S, Kaur T, Kumar S, Lakhanpal D, Lakhman SS, Kaur G. Middle age onset short-term intermittent fasting dietary restriction prevents brain function impairments in male Wistar rats. Biogerontology. 2015 Dec;16(6):775-88. doi: 10.1007/s10522-015-9603-y. Epub 2015 Aug 30. PubMed PMID: 26318578.
Tinsley GM, La Bounty PM. Effects of intermittent fasting on body composition and clinical health markers in humans. Nutr Rev. 2015 Oct;73(10):661-74. doi: 10.1093/nutrit/nuv041. Epub 2015 Sep 15. Review. PubMed PMID: 26374764.
Jane L, Atkinson G, Jaime V, Hamilton S, Waller G, Harrison S. Intermittent fasting interventions for the treatment of overweight and obesity in adults aged 18 years and over: a systematic review protocol. JBI Database System Rev Implement Rep. 2015 Oct;13(10):60-8. doi: 10.11124/jbisrir-2015-2363. PubMed PMID: 26571283.
Patterson RE, Laughlin GA, LaCroix AZ, Hartman SJ, Natarajan L, Senger CM, Martínez ME, Villaseñor A, Sears DD, Marinac CR, Gallo LC. Intermittent Fasting and Human Metabolic Health. J Acad Nutr Diet. 2015 Aug;115(8):1203-12. doi: 10.1016/j.jand.2015.02.018. Epub 2015 Apr 6. PubMed PMID: 25857868; PubMed Central PMCID: PMC4516560.
Horne BD, Muhlestein JB, Anderson JL. Health effects of intermittent fasting: hormesis or harm? A systematic review. Am J Clin Nutr. 2015 Aug;102(2):464-70. doi: 10.3945/ajcn.115.109553. Epub 2015 Jul 1. Review. PubMed PMID: 26135345.
Carey SK, Conchin S, Bloomfield-Stone S. A qualitative study into the impact of fasting within a large tertiary hospital in Australia--the patients' perspective. J Clin Nurs. 2015 Jul;24(13-14):1946-54. doi: 10.1111/jocn.12847. Epub 2015 May 11. PubMed PMID: 25959390.
Johnstone A. Fasting for weight loss: an effective strategy or latest dieting trend? Int J Obes (Lond). 2015 May;39(5):727-33. doi: 10.1038/ijo.2014.214. Epub 2014 Dec 26. Review. PubMed PMID: 25540982.
Baumeier C, Kaiser D, Heeren J, Scheja L, John C, Weise C, Eravci M, Lagerpusch M, Schulze G, Joost HG, Schwenk RW, Schürmann A. Caloric restriction and intermittent fasting alter hepatic lipid droplet proteome and diacylglycerol species and prevent diabetes in NZO mice. Biochim Biophys Acta. 2015 May;1851(5):566-76. doi: 10.1016/j.bbalip.2015.01.013. Epub 2015 Jan 31. PubMed PMID: 25645620.
Wegman MP, Guo MH, Bennion DM, Shankar MN, Chrzanowski SM, Goldberg LA, Xu J, Williams TA, Lu X, Hsu SI, Anton SD, Leeuwenburgh C, Brantly ML. Practicality of intermittent fasting in humans and its effect on oxidative stress and genes related to aging and metabolism. Rejuvenation Res. 2015 Apr;18(2):162-72. doi: 10.1089/rej.2014.1624. PubMed PMID: 25546413; PubMed Central PMCID: PMC4403246.
Samad F, Qazi F, Pervaiz MB, Kella DK, Mansoor M, Osmani BZ, Mir F, Kadir MM. EFFECTS OF RAMADAN FASTING ON BLOOD PRESSURE IN NORMOTENSIVE MALES. J Ayub Med Coll Abbottabad. 2015 Apr-Jun;27(2):338-42. PubMed PMID: 26411111.
Bemben DA, Sharma-Ghimire P, Chen Z, Kim E, Kim D, Bemben MG. Effects of whole-body vibration on acute bone turnover marker responses to resistance exercise in young men. J Musculoskelet Neuronal Interact. 2015 Mar;15(1):23-31. PubMed PMID: 25730649.
Lankelma J, Kooi B, Krab K, Dorsman JC, Joenje H, Westerhoff HV. A reason for intermittent fasting to suppress the awakening of dormant breast tumors. Biosystems. 2015 Jan;127:1-6. doi: 10.1016/j.biosystems.2014.11.001. Epub 2014 Nov 4. PubMed PMID: 25448890.
Chausse B, Vieira-Lara MA, Sanchez AB, Medeiros MH, Kowaltowski AJ. Intermittent fasting results in tissue-specific changes in bioenergetics and redox state. PLoS One. 2015 Mar 6;10(3):e0120413. doi: 10.1371/journal.pone.0120413. eCollection 2015. PubMed PMID: 25749501; PubMed Central PMCID: PMC4352038.
Godar RJ, Ma X, Liu H, Murphy JT, Weinheimer CJ, Kovacs A, Crosby SD, Saftig P, Diwan A. Repetitive stimulation of autophagy-lysosome machinery by intermittent fasting preconditions the myocardium to ischemia-reperfusion injury. Autophagy. 2015;11(9):1537-60. doi: 10.1080/15548627.2015.1063768. PubMed PMID: 26103523; PubMed Central PMCID: PMC4590628.
Barnosky AR, Hoddy KK, Unterman TG, Varady KA. Intermittent fasting vs daily calorie restriction for type 2 diabetes prevention: a review of human findings. Transl Res. 2014 Oct;164(4):302-11. doi: 10.1016/j.trsl.2014.05.013. Epub 2014 Jun 12. Review. PubMed PMID: 24993615.
Fann DY, Santro T, Manzanero S, Widiapradja A, Cheng YL, Lee SY, Chunduri P, Jo DG, Stranahan AM, Mattson MP, Arumugam TV. Intermittent fasting attenuates inflammasome activity in ischemic stroke. Exp Neurol. 2014 Jul;257:114-9. doi: 10.1016/j.expneurol.2014.04.017. Epub 2014 May 5. PubMed PMID: 24805069.
Aly SM. Role of intermittent fasting on improving health and reducing diseases. Int J Health Sci (Qassim). 2014 Jul;8(3):V-VI. PubMed PMID: 25505868; PubMed Central PMCID: PMC4257368.
Vasconcelos AR, Yshii LM, Viel TA, Buck HS, Mattson MP, Scavone C, Kawamoto EM. Intermittent fasting attenuates lipopolysaccharide-induced neuroinflammation and memory impairment. J Neuroinflammation. 2014 May 6;11:85. doi: 10.1186/1742-2094-11-85. PubMed PMID: 24886300; PubMed Central PMCID: PMC4041059.
Manzanero S, Erion JR, Santro T, Steyn FJ, Chen C, Arumugam TV, Stranahan AM. Intermittent fasting attenuates increases in neurogenesis after ischemia and reperfusion and improves recovery. J Cereb Blood Flow Metab. 2014 May;34(5):897-905. doi: 10.1038/jcbfm.2014.36. Epub 2014 Feb 19. PubMed PMID: 24549184; PubMed Central PMCID: PMC4013772.
Godínez-Victoria M, Campos-Rodriguez R, Rivera-Aguilar V, Lara-Padilla E, Pacheco-Yepez J, Jarillo-Luna RA, Drago-Serrano ME. Intermittent fasting promotes bacterial clearance and intestinal IgA production in Salmonella typhimurium-infected mice. Scand J Immunol. 2014 May;79(5):315-24. doi: 10.1111/sji.12163. PubMed PMID: 24612255.
Dorighello GG, Rovani JC, Luhman CJ, Paim BA, Raposo HF, Vercesi AE, Oliveira HC. Food restriction by intermittent fasting induces diabetes and obesity and aggravates spontaneous atherosclerosis development in hypercholesterolaemic mice. Br J Nutr. 2014 Mar 28;111(6):979-86. doi: 10.1017/S0007114513003383. Epub 2013 Nov 1. PubMed PMID: 24176004.
Westbrook R, Bonkowski MS, Arum O, Strader AD, Bartke A. Metabolic alterations due to caloric restriction and every other day feeding in normal and growth hormone receptor knockout mice. J Gerontol A Biol Sci Med Sci. 2014 Jan;69(1):25-33. doi: 10.1093/gerona/glt080. Epub 2013 Jul 5. PubMed PMID: 23833202; PubMed Central PMCID: PMC3859362.
Alzoghaibi MA, Pandi-Perumal SR, Sharif MM, BaHammam AS. Diurnal intermittent fasting during Ramadan: the effects on leptin and ghrelin levels. PLoS One. 2014 Mar 17;9(3):e92214. doi: 10.1371/journal.pone.0092214. eCollection 2014. PubMed PMID: 24637892; PubMed Central PMCID: PMC3956913.
Lv M, Zhu X, Wang H, Wang F, Guan W. Roles of caloric restriction, ketogenic diet and intermittent fasting during initiation, progression and metastasis of cancer in animal models: a systematic review and meta-analysis. PLoS One. 2014 Dec 11;9(12):e115147. doi: 10.1371/journal.pone.0115147. eCollection 2014. PubMed PMID: 25502434; PubMed Central PMCID: PMC4263749.
Teng NI, Shahar S, Rajab NF, Manaf ZA, Johari MH, Ngah WZ. Improvement of metabolic parameters in healthy older adult men following a fasting calorie restriction intervention. Aging Male. 2013 Dec;16(4):177-83. doi: 10.3109/13685538.2013.832191. Epub 2013 Sep 17. PubMed PMID: 24044618.
Collier R. Intermittent fasting: the science of going without. CMAJ. 2013 Jun 11;185(9):E363-4. doi: 10.1503/cmaj.109-4451. Epub 2013 Apr 8. PubMed PMID: 23569168; PubMed Central PMCID: PMC3680567.
Pilon B. Intermittent fasting: five quick questions with fasting expert Brad Pilon. Interview by Roger Collier. CMAJ. 2013 Jun 11;185(9):E362. doi: 10.1503/cmaj.109-4438. Epub 2013 Apr 15. PubMed PMID: 23589435; PubMed Central PMCID: PMC3680566.
Collier R. Intermittent fasting: the next big weight loss fad. CMAJ. 2013 May 14;185(8):E321-2. doi: 10.1503/cmaj.109-4437. Epub 2013 Mar 25. PubMed PMID: 23529969; PubMed Central PMCID: PMC3652955.
Azevedo FR, Ikeoka D, Caramelli B. Effects of intermittent fasting on metabolism in men. Rev Assoc Med Bras (1992). 2013 Mar-Apr;59(2):167-73. doi: 10.1016/j.ramb.2012.09.003. Review. PubMed PMID: 23582559.
Li L, Wang Z, Zuo Z. Chronic intermittent fasting improves cognitive functions and brain structures in mice. PLoS One. 2013 Jun 3;8(6):e66069. doi: 10.1371/journal.pone.0066069. Print 2013. PubMed PMID: 23755298; PubMed Central PMCID: PMC3670843.
Hussin NM, Shahar S, Teng NI, Ngah WZ, Das SK. Efficacy of fasting and calorie restriction (FCR) on mood and depression among ageing men. J Nutr Health Aging. 2013;17(8):674-80. doi: 10.1007/s12603-013-0344-9. PubMed PMID: 24097021.
Hammouda O, Chtourou H, Aloui A, Chahed H, Kallel C, Miled A, Chamari K, Chaouachi A, Souissi N. Concomitant effects of Ramadan fasting and time-of-day on apolipoprotein AI, B, Lp-a and homocysteine responses during aerobic exercise in Tunisian soccer players. PLoS One. 2013 Nov 11;8(11):e79873. doi: 10.1371/journal.pone.0079873. eCollection 2013. PubMed PMID: 24244572; PubMed Central PMCID: PMC3823586.
Faris MA, Kacimi S, Al-Kurd RA, Fararjeh MA, Bustanji YK, Mohammad MK, Salem ML. Intermittent fasting during Ramadan attenuates proinflammatory cytokines and immune cells in healthy subjects. Nutr Res. 2012 Dec;32(12):947-55. doi: 10.1016/j.nutres.2012.06.021. Epub 2012 Oct 4. PubMed PMID: 23244540.
Kroeger CM, Klempel MC, Bhutani S, Trepanowski JF, Tangney CC, Varady KA. Improvement in coronary heart disease risk factors during an intermittent fasting/calorie restriction regimen: Relationship to adipokine modulations. Nutr Metab (Lond). 2012 Oct 31;9(1):98. doi: 10.1186/1743-7075-9-98. PubMed PMID: 23113919; PubMed Central PMCID: PMC3514278.
Singh R, Lakhanpal D, Kumar S, Sharma S, Kataria H, Kaur M, Kaur G. Late-onset intermittent fasting dietary restriction as a potential intervention to retard age-associated brain function impairments in male rats. Age (Dordr). 2012 Aug;34(4):917-33. doi: 10.1007/s11357-011-9289-2. Epub 2011 Aug 23. PubMed PMID: 21861096; PubMed Central PMCID: PMC3682068.
Arguin H, Dionne IJ, Sénéchal M, Bouchard DR, Carpentier AC, Ardilouze JL, Tremblay A, Leblanc C, Brochu M. Short- and long-term effects of continuous versus intermittent restrictive diet approaches on body composition and the metabolic profile in overweight and obese postmenopausal women: a pilot study. Menopause. 2012 Aug;19(8):870-6. PubMed PMID: 22735163.
Karbowska J, Kochan Z. Intermittent fasting up-regulates Fsp27/Cidec gene expression in white adipose tissue. Nutrition. 2012 Mar;28(3):294-9. doi: 10.1016/j.nut.2011.06.009. Epub 2011 Oct 12. PubMed PMID: 21996045.
Belkacemi L, Selselet-Attou G, Hupkens E, Nguidjoe E, Louchami K, Sener A, Malaisse WJ. Intermittent fasting modulation of the diabetic syndrome in streptozotocin-injected rats. Int J Endocrinol. 2012;2012:962012. doi: 10.1155/2012/962012. Epub 2012 Jan 12. PubMed PMID: 22291702; PubMed Central PMCID: PMC3265126.
Faris MA, Hussein RN, Al-Kurd RA, Al-Fararjeh MA, Bustanji YK, Mohammad MK. Impact of ramadan intermittent fasting on oxidative stress measured by urinary 15-f(2t)-isoprostane. J Nutr Metab. 2012;2012:802924. doi: 10.1155/2012/802924. Epub 2012 Oct 22. PubMed PMID: 23150812; PubMed Central PMCID: PMC3485525.
Thompson HJ, McTiernan A. Weight cycling and cancer: weighing the evidence of intermittent caloric restriction and cancer risk.Cancer Prev Res (Phila). 2011 Nov;4(11):1736-42. doi: 10.1158/1940-6207.CAPR-11-0133. Epub 2011 Oct 7. Review. PubMed PMID: 21982873; PubMed Central PMCID: PMC3208747.
Razzak RL, Abu-Hozaifa BM, Bamosa AO, Ali NM. Assessment of enhanced endothelium-dependent vasodilation by intermittent fasting in Wistar albino rats. Indian J Physiol Pharmacol. 2011 Oct-Dec;55(4):336-42. PubMed PMID: 23362726.
Harvie MN, Pegington M, Mattson MP, Frystyk J, Dillon B, Evans G, Cuzick J, Jebb SA, Martin B, Cutler RG, Son TG, Maudsley S, Carlson OD, Egan JM, Flyvbjerg A, Howell A. The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women. Int J Obes (Lond). 2011 May;35(5):714-27. doi: 10.1038/ijo.2010.171. Epub 2010 Oct 5. PubMed PMID: 20921964; PubMed Central PMCID: PMC3017674.
Lu J, E L, Wang W, Frontera J, Zhu H, Wang WT, Lee P, Choi IY, Brooks WM, Burns JM, Aires D, Swerdlow RH. Alternate day fasting impacts the brain insulin-signaling pathway of young adult male C57BL/6 mice. J Neurochem. 2011 Apr;117(1):154-63. doi: 10.1111/j.1471-4159.2011.07184.x. Epub 2011 Feb 9. PubMed PMID: 21244426; PubMed Central PMCID: PMC3055925.
Jeong MA, Plunet W, Streijger F, Lee JH, Plemel JR, Park S, Lam CK, Liu J, Tetzlaff W. Intermittent fasting improves functional recovery after rat thoracic contusion spinal cord injury. J Neurotrauma. 2011 Mar;28(3):479-92. doi: 10.1089/neu.2010.1609. PubMed PMID: 21219083; PubMed Central PMCID: PMC3119327.
Belkacemi L, Selselet-Attou G, Bulur N, Louchami K, Sener A, Malaisse WJ. Intermittent fasting modulation of the diabetic syndrome in sand rats. III. Post-mortem investigations. Int J Mol Med. 2011 Jan;27(1):95-102. doi: 10.3892/ijmm.2010.556. Epub 2010 Nov 10. PubMed PMID: 21069262.
Thomas JA 2nd, Antonelli JA, Lloyd JC, Masko EM, Poulton SH, Phillips TE, Pollak M, Freedland SJ. Effect of intermittent fasting on prostate cancer tumor growth in a mouse model. Prostate Cancer Prostatic Dis. 2010 Dec;13(4):350-5. doi: 10.1038/pcan.2010.24. Epub 2010 Aug 24. PubMed PMID: 20733612.
Belkacemi L, Selselet-Attou G, Louchami K, Sener A, Malaisse WJ. Intermittent fasting modulation of the diabetic syndrome in sand rats. II. In vivo investigations. Int J Mol Med. 2010 Nov;26(5):759-65. PubMed PMID: 20878099.
Tajes M, Gutierrez-Cuesta J, Folch J, Ortuño-Sahagun D, Verdaguer E, Jiménez A, Junyent F, Lau A, Camins A, Pallàs M. Neuroprotective role of intermittent fasting in senescence-accelerated mice P8 (SAMP8). Exp Gerontol. 2010 Sep;45(9):702-10. doi: 10.1016/j.exger.2010.04.010. Epub 2010 May 9. PubMed PMID: 20460146.
Buschemeyer WC 3rd, Klink JC, Mavropoulos JC, Poulton SH, Demark-Wahnefried W, Hursting SD, Cohen P, Hwang D, Johnson TL, Freedland SJ. Effect of intermittent fasting with or without caloric restriction on prostate cancer growth and survival in SCID mice. Prostate. 2010 Jul 1;70(10):1037-43. doi: 10.1002/pros.21136. PubMed PMID: 20166128.
Wan R, Ahmet I, Brown M, Cheng A, Kamimura N, Talan M, Mattson MP. Cardioprotective effect of intermittent fasting is associated with an elevation of adiponectin levels in rats. J Nutr Biochem. 2010 May;21(5):413-7. doi: 10.1016/j.jnutbio.2009.01.020. Epub 2009 May 7. PubMed PMID: 19423320; PubMed Central PMCID: PMC2854256.
Katare RG, Kakinuma Y, Arikawa M, Yamasaki F, Sato T. Chronic intermittent fasting improves the survival following large myocardial ischemia by activation of BDNF/VEGF/PI3K signaling pathway. J Mol Cell Cardiol. 2009 Mar;46(3):405-12. doi: 10.1016/j.yjmcc.2008.10.027. Epub 2008 Nov 12. PubMed PMID: 19059263.
Salim S, Farooq N, Priyamvada S, Asghar M, Khundmiri SJ, Khan S, Khan F, Yusufi AN. Influence of Ramadan-type fasting on carbohydrate metabolism, brush border membrane enzymes and phosphate transport in rat kidney used as a model. Br J Nutr. 2007 Nov;98(5):984-90. Epub 2007 Sep 3. PubMed PMID: 17764602.
Donato J Jr, Pedrosa RG, de Araújo JA Jr, Pires IS, Tirapegui J. Effects of leucine and phenylalanine supplementation during intermittent periods of food restriction and refeeding in adult rats. Life Sci. 2007 Jun 13;81(1):31-9. Epub 2007 Apr 24. PubMed PMID: 17512018.
Halagappa VK, Guo Z, Pearson M, Matsuoka Y, Cutler RG, Laferla FM, Mattson MP. Intermittent fasting and caloric restriction ameliorate age-related behavioral deficits in the triple-transgenic mouse model of Alzheimer's disease. Neurobiol Dis. 2007 Apr;26(1):212-20. Epub 2007 Jan 13. PubMed PMID: 17306982.
Tikoo K, Tripathi DN, Kabra DG, Sharma V, Gaikwad AB. Intermittent fasting prevents the progression of type I diabetic nephropathy in rats and changes the expression of Sir2 and p53. FEBS Lett. 2007 Mar 6;581(5):1071-8. Epub 2007 Feb 14. PubMed PMID: 17316625.
Martin B, Mattson MP, Maudsley S. Caloric restriction and intermittent fasting: two potential diets for successful brain aging. Ageing Res Rev. 2006 Aug;5(3):332-53. Epub 2006 Aug 8. Review. PubMed PMID: 16899414; PubMed Central PMCID: PMC2622429.
Lee J, Kim SJ, Son TG, Chan SL, Mattson MP. Interferon-gamma is up-regulated in the hippocampus in response to intermittent fasting and protects hippocampal neurons against excitotoxicity. J Neurosci Res. 2006 Jun;83(8):1552-7. PubMed PMID: 16521127.
Mager DE, Wan R, Brown M, Cheng A, Wareski P, Abernethy DR, Mattson MP. Caloric restriction and intermittent fasting alter spectral measures of heart rate and blood pressure variability in rats. FASEB J. 2006 Apr;20(6):631-7. PubMed PMID: 16581971.
Barboza PS, Hume ID. Physiology of intermittent feeding: integrating responses of vertebrates to nutritional deficit and excess.Physiol Biochem Zool. 2006 Mar-Apr;79(2):250-64. Epub 2006 Feb 7. PubMed PMID: 16555185.
Tapia PC. Sublethal mitochondrial stress with an attendant stoichiometric augmentation of reactive oxygen species may precipitate many of the beneficial alterations in cellular physiology produced by caloric restriction, intermittent fasting, exercise and dietary phytonutrients: "Mitohormesis" for health and vitality. Med Hypotheses. 2006;66(4):832-43. Epub 2005 Oct 18. PubMed PMID: 16242247.
Michalsen A, Riegert M, Lüdtke R, Bäcker M, Langhorst J, Schwickert M, Dobos GJ. Mediterranean diet or extended fasting's influence on changing the intestinal microflora, immunoglobulin A secretion and clinical outcome in patients with rheumatoid arthritis and fibromyalgia: an observational study. BMC Complement Altern Med. 2005 Dec 22;5:22. PubMed PMID: 16372904; PubMed Central PMCID: PMC1352378.
Halberg N, Henriksen M, Söderhamn N, Stallknecht B, Ploug T, Schjerling P, Dela F. Effect of intermittent fasting and refeeding on insulin action in healthy men. J Appl Physiol (1985). 2005 Dec;99(6):2128-36. Epub 2005 Jul 28. PubMed PMID: 16051710.
Ahmet I, Wan R, Mattson MP, Lakatta EG, Talan M. Cardioprotection by intermittent fasting in rats. Circulation. 2005 Nov 15;112(20):3115-21. Epub 2005 Nov 7. PubMed PMID: 16275865.
Descamps O, Riondel J, Ducros V, Roussel AM. Mitochondrial production of reactive oxygen species and incidence of age-associated lymphoma in OF1 mice: effect of alternate-day fasting. Mech Ageing Dev. 2005 Nov;126(11):1185-91. PubMed PMID: 16126250.
Mattson MP, Wan R. Beneficial effects of intermittent fasting and caloric restriction on the cardiovascular and cerebrovascular systems. J Nutr Biochem. 2005 Mar;16(3):129-37. Review. PubMed PMID: 15741046.
Aksungar FB, Eren A, Ure S, Teskin O, Ates G. Effects of intermittent fasting on serum lipid levels, coagulation status and plasma homocysteine levels. Ann Nutr Metab. 2005 Mar-Apr;49(2):77-82. Epub 2005 Mar 29. PubMed PMID: 15802901.
Wan R, Camandola S, Mattson MP. Intermittent fasting and dietary supplementation with 2-deoxy-D-glucose improve functional and metabolic cardiovascular risk factors in rats. FASEB J. 2003 Jun;17(9):1133-4. Epub 2003 Apr 22. PubMed PMID: 12709404.
Anson RM, Guo Z, de Cabo R, Iyun T, Rios M, Hagepanos A, Ingram DK, Lane MA, Mattson MP. Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake. Proc Natl Acad Sci U S A. 2003 May 13;100(10):6216-20. Epub 2003 Apr 30. PubMed PMID: 12724520; PubMed Central PMCID: PMC156352.
Rocha NS, Barbisan LF, de Oliveira ML, de Camargo JL. Effects of fasting and intermittent fasting on rat hepatocarcinogenesis induced by diethylnitrosamine. Teratog Carcinog Mutagen. 2002;22(2):129-38. PubMed PMID: 11835290.
Pedersen CR, Hagemann I, Bock T, Buschard K. Intermittent feeding and fasting reduces diabetes incidence in BB rats.Autoimmunity. 1999;30(4):243-50. PubMed PMID: 10524500.
Krízová E, Simek V. Influence of intermittent fasting and high-fat diet on morphological changes of the digestive system and on changes of lipid metabolism in the laboratory mouse. Physiol Res. 1996;45(2):145-51. PubMed PMID: 9496764.
Nir I, Harvey S, Nitsan Z, Pinchasov Y, Chadwick A. Effect of intermittent feeding on blood plasma growth hormone and prolactin in chickens of a heavy breed. Br Poult Sci. 1983 Jan;24(1):63-70. PubMed PMID: 6831277.
Kozubík A, Pospísil M. Protective effect of intermittent fasting on the mortality of gamma-irradiated mice. Strahlentherapie. 1982 Dec;158(12):734-8. PubMed PMID: 6761903.
Vondra K, Rath R, Bass A, Kuzela L, Slabochová Z. [Prolonged intermittent fasting in obese women. Effect on activity of energy metabolism enzymes, glycogen concentration, protein and DNA in skeletal muscle (author's transl)]. Cas Lek Cesk. 1976 Apr;115(15):454-7. Czech. PubMed PMID: 1268896.
Simek V. Energy metabolism of golden hamsters adapted to intermittent fasting: influence of season and sex. Physiol Bohemoslov. 1974;23(5):437-46. PubMed PMID: 4278700.
Kreisler K, Petrásek R. Changes of carbohydrate metabolism during satiety and after varying periods of fasting in rats adapted to intermittent starvation. Physiol Bohemoslov. 1974;23(3):271-6. PubMed PMID: 4280593.
Ruckebusch M, Ferré JP. [Digestive tract alterations connected with intermittent fasting in rats]. Z Zellforsch Mikrosk Anat. 1973 Jun 20;140(1):1552-6. French. PubMed PMID: 4730780.
Stewart WK, Fleming LW, Robertson PC. Massive obesity treated by intermittent fasting. A metabolic and clinical study. Am J Med. 1966 Jun;40(6):967-86. PubMed PMID: 5936189.
Intermittent food restriction. Nutr Rev. 1966 Mar;24(3):83-6. Review. PubMed PMID: 5324330.
Schless GL, Duncan GG. The beneficial effect of intermittent total fasts on the glucose tolerance in obese diabetic patients.Metabolism. 1966 Feb;15(2):98-102. PubMed PMID: 5901780.
Duncan GG, Hunscher MA, Cristofori FC, Duncan TG, Schless GL. Intermittent total fasts and obesity; indications, results and preventable hazards. Postgrad Med. 1965 Nov;38(5):523-35. PubMed PMID: 5833523.
DUNCAN GG. INTERMITTENT FASTS IN THE CORRECTION AND CONTROL OF INTRACTABLE OBESITY. Trans Am Clin Climatol Assoc. 1962;74:121-9. PubMed PMID: 14047310; PubMed Central PMCID: PMC2249073.
INTERMITTENT fasting and longevity in rats. Nutr Rev. 1946 Jul;4(7):218. PubMed PMID: 20992558.
CARLSON AJ, HOELZEL F. Apparent prolongation of the life span of rats by intermittent fasting. J Nutr. 1946 Mar;31:363-75. PubMed PMID: 21021020.
This is likely to be the most controversial step I am recommending. For the past 30-plus years we have been hearing about the evils of dietary fat in general and of saturated fat in particular. This led to the "low-fat" food craze and a constant barrage of "healthy" low-fat manufactured foods.
Unfortunately, during this time the rates of obesity, type 2 diabetes and cardiovascular disease steadily increased.
What is happening here?
To conduct good science, a researcher develops a hypothesis, but then designs experiments to disprove the hypothesis. If unable to disprove the hypothesis, it stands. This process is notably different than how the nutritional studies that led to the USDA guidelines were conducted. Here the researchers developed a hypothesis but then selectively presented data that would support their hypothesis and excluded all non-supporting data. This is not science. Nina Teicholz presents a well supported indictment of the process that ultimately led to the flawed USDA guidelines in her excellent book "The Big Fat Surprise." I highly recommend reading her book.
In a previous blog posting, I suggested the constant exposure to dietary carbohydrates causes chronically elevated insulin levels which then leads to the chronic diseases of the modern world. It appears the dietary fat recommendations may have contributed to this both directly and indirectly. Because there are only 3 macro nutrients (carbohydrates, proteins, and fats), by reducing fat intake, we must increase the intake of another macronutrient. So clearly, reducing fat intake will lead to relative increases in other macronutrients. Remember the low-fat processed food explosion? Here the industrial food companies often increased sugar content of foods to maintain palatability when fats were eliminated. As a result we ate more carbohydrates as we reduced dietary fats. Because dietary fat leaves the gastrointestinal tract more slowly, increased satiety results. When fat intake is low, our hunger often returns soon after eating, leading to snacking on....more low-fat food products. These are indirect ways reducing dietary fat can be counterproductive.
It also appears the USDA dietary fat recommendations may be contributing to disease directly.
An in-depth discussion of organic chemistry is beyond the scope of this blog posting, however it is important to understand some basic concepts. Dietary fat consists of a chain of carbon atoms. Each carbon atom has the ability to make 4 bonds. If each carbon in the chain has 4 single bonds, the fat is referred to as saturated. If a pair of carbon atoms are linked with a double bond, the fat is called monounsaturated. If multiple carbon atoms are linked by double bonds, it is a polyunsaturated fat. Double bonds are inherently more reactive than single bonds and as we move from saturated, to monounsaturated, to polyunsaturated, the fatty acid becomes increasingly unstable.
Heat, oxygen and light can all damage the carbon chain. This is of particular importance when cooking. Aldehydes and trans-fats can be created by heating polyunsaturated fats. One example of an aldehyde is formaldehyde, a chemical used to preserve biological tissues (remember high school biology class?). Aldehydes are very reactive chemicals and are believed to cause inflammation and oxidative stress to our bodies. This could be a mechanism by which polyunsaturated fat consumption may be contributing to disease.
Traditionally, saturated fats were used for cooking. Once saturated fat was maligned by the USDA, industrially created trans-fats were introduced as a substitute. Unfortunately, trans-fats are now known to be much more detrimental to our health than any naturally occurring fats. Examples include vegetable shortening, and anything that contains the words "partially hydrogenated." Trans-fats raise our LDL cholesterol (bad cholesterol) and reduce our HDL (good cholesterol). These products should be considered poisonous and be completely avoided.
Cooking with polyunsaturated oils became the standard, but as previously discussed, produces harmful byproducts than can cause inflammation, and can contribute to heart disease and even cancer.
Which brings us back to saturated fat. With no double bonds to break, saturated fat tends to be much more stable for cooking. It appears our ancestors already figured this out. Coconut oil is a good example of a cooking oil that is rich in saturated fat. Animal fat tends to be relatively rich in saturated fat as well. Tallow (beef fat) contains about 50% saturated fat, and about 45% monounsaturated fat, the remainder is polyunsaturated. Butter contains about 66% saturated fat, and about 25% monounsaturated fat. These are all good fats to cook with. It is widely known that exercise and moderate alcohol consumption can raise our HDL (good cholesterol). Much less widely known, an even more powerful way to raise your HDL (good cholesterol) is through the consumption of saturated fat. Some people will experience a moderate increase in total cholesterol levels when increasing their consumption of saturated fat. The cardiovascular risk profile will generally be significantly improved, but your individual response should be monitored.
Olive oil contains over 70% monounsaturated fat. Although probably acceptable for low temperature cooking, I recommend buying a high quality brand that is packaged in a dark glass container and consuming it uncooked. It can be poured over cooked food and used on salads liberally. This and other sources of monounsaturated oil like macadamia nuts and avocados should be eaten routinely.
Polyunsaturated fats must be treated carefully. They should not be heated, and only consumed when fresh. 2 main subtypes are referred to as omega 3 and omega 6 fats based on the location of their double bonds. These are essential fatty acids, meaning our bodies can not manufacture them, but requires them for health. The dose needed is relatively low and can easily be obtained through a proper diet. The standard American diet is very high in omega 6 fats, (which tend to cause inflammation) and is often deficient in omega 3 fats, (which tend to reduce inflammation). Once again we are promoting inflammation and chronic disease. We should try to minimize overconsumption of omega 6 fats and seek out fresh sources of omega 3 fats. Excellent sources of omega 3 fats are wild caught salmon, canned sardines, and other seafood. One of the main reasons Americans consume too much omega 6 fat is that soybean oil is ubiquitous and it contains 50% omega 6 polyunsaturated fat. Much of this is partially hydrogenated- which is even worse. Other vegetable oils have infiltrated our manufactured food products and are very difficult to avoid. Please read labels and avoid any foods that contain soybean, corn, sunflower or cottonseed oils.
Because I am recommending a low-carbohydrate, moderate-protein, high-fat diet, most of our calories (50-80%) will be coming from fat. These fats end up becoming incorporated into our cell membranes and will influence how our body functions. We want these fats to be undamaged and to promote health, not lead to inflammation and subsequent chronic diseases. It is important to read labels, avoid harmful fats, and choose the best fats to cook with.
Prior to making a dietary change, I recommend getting a baseline lipid panel. While the vast majority of us will experience a dramatic improvement in our cardiovascular risk profile (increased HDL, decreased triglycerides, decreased body weight, and reduced waist circumference) when choosing to avoid refined carbohydrates and increase dietary fat consumption (as outlined above), our bodies don't all work identically. It is important to monitor your progress and adjust as needed.
A common misconception many people have is that people on a low-carbohydrate diet only eat meat. Although "meat only" diets have been studied, and actually have been found to be safe, this is not at all what I suggest. In fact, a well formulated low-carbohydrate diet should really be considered a low to moderate protein diet. Again, we need to strive to get the majority of our calories from fat. I will discuss healthy fats in the next article.
Proteins are made up of chains of amino acids. The process of digestion breaks ingested proteins down into amino acids. These amino acids can then be used by your body to make specific proteins needed structurally (bone, muscle) and to support cellular function via signaling and enzymatic activity.
Amino acids can also be used for energy or stored as body fat. Of the 20 amino acids used in the human body, 9 are essential. This means they must be eaten. The body can fabricate the other 11 if needed. A complete dietary protein contains all of the essential amino acids. Meat is a complete protein. Incomplete proteins can also be eaten in combination to supply all essential amino acids. This is how vegetarians can ensure proper protein intake.
The amount of protein an individual needs is based on the normal turnover of proteins in their body each day. Larger body mass and an increased activity level require increased protein intake. Eating protein beyond this point is not beneficial and could significantly undermine weight-loss efforts.
Some amino acids will cause an insulin release. As I discussed in the last blog posting, we are attempting to minimize our insulin levels to allow our body fat to be mobilized for energy, and to stop the blood sugar instability that leads to cravings. For these reasons, it is best to eat the proper amount of protein (a moderate level) for your body and activity level.
How much is that? Adequate protein intake for most people is 0.3-0.8 grams of protein per pound of ideal body weight. I often use 0.5 grams as a simple rule of thumb. So this means if your ideal body weight is 150 pounds, you should strive for about 75g of protein over the day. To maximize weight loss, especially if not exercising, aim for the lower end at about 50 grams. Some body-builders consume several times this amount of protein, but their goals are completely different than ours. We are not trying to pack on as much muscle as possible, we are trying to burn body fat for energy while maintaining our muscle mass and optimizing the function of our cells.
To put this in perspective, a six ounce steak has about 50 grams of complete protein. A five ounce serving of salmon will deliver 36 grams of protein. A single large egg or a handful of almonds each contains 6 grams of protein. One slice of cheddar cheese will provide 7 grams of protein. Vegetables also contain protein, but at a much lower concentration. As I will further develop in the future, my recommended diet is not vegetarian, but it does contain lots of vegetables. The biggest volume of food you should be eating is non-starchy vegetables, while the biggest source of calories will ultimately be dietary fats. When eaten in significant quantity, vegetables will actually end up supplying a reasonable amount of protein.
A common misconception that has been beaten into our heads is that "lean" meats are best. We have been trained to fear fat. For this reason, many people instinctively think of chicken breast, or tuna as excellent protein sources. And they are. But not for optimal body-weight, health, and performance. Why is this? Because they contain no fat. Just 3 ounces of cooked tuna supplies 25 grams of protein, but only 5 grams of fat. Even worse, a half of a chicken breast contains 27 grams of protein and just 3 grams of fat.
Remember, we want our body to burn fat, thus we must eat fat.
Take home points:
1: Low-carbohydrate does not automatically mean high protein.
2: It is easy to supply your body with adequate protein by consuming a variety of foods.
3: Don't fall into the "lean meat" trap. Lean meats over-supply protein, and under-supply fat. Choose the fattiest cuts of meat and don't feel guilty.
4: When you do choose to eat a lean meat like chicken or non-fatty fish, keep the portion size small, and feel free to add plenty of butter, cream, or olive oil to the sauce.
In the next few postings, I will break my nutritional recommendations down into a few simple steps.
First, it is important to understand that there are only 3 actual food groups. These are the macronutrients. The 3 macronutrients are fats, proteins, and carbohydrates. Each can provide our body with energy. In addition to potentially supplying energy, protein also provides the building blocks that make up the structure of our body. Technically, our body can also obtain energy when it metabolizes alcohol, but this should not make up a significant part of a healthy diet so we will exclude it for now.
Carbohydrates are sugars, starches, and fiber. Fiber is the undigestible part of plants and grains and does not provide energy to your body. Whether consumed in the form of sugar or starch, carbohydrates are all broken down, or digested, into sugars. This happens very rapidly in your gastrointestinal tract. Starch is just a long chain of sugar molecules linked together. This linkage is rapidly broken. You can test this by chewing a saltine cracker and not swallowing it. After a few minutes in your mouth the enzyme in your saliva (salivary amylase) begins breaking the starch down into sugar. This is why the chewed cracker begins tasting sweet when held in your mouth.
As far as your body is concerned, all absorbed carbohydrates are sugar.
When sugar is absorbed, your blood sugar level rises. Although some glucose (sugar) in you blood is necessary, too much is toxic. Your body responds by secreting insulin from the pancreas. This drives the sugar into your cells to provide energy. When your cells have enough supply of sugar, the excess can be stored as glycogen. Glycogen is primarily stored in the liver and muscles. We can only store about a days worth of energy in this form. When glycogen levels are adequate, excess blood sugar is then stored as body fat.
The modern diet tends to be rich in carbohydrates, especially processed, refined carbohydrates. As a result of constant exposure to incoming sugars, our body responds by increasing (up-regulating) the carbohydrate metabolizing system. Studies have suggested many people have fasting hyperinsulinemia (abnormally elevated insulin levels beyond what is needed to deal with a recent meal). This can result in 2 major issues: 1- extreme hunger, 2- inability to mobilize body fat for energy.
Since insulin lowers blood sugar, when your pancreas, in anticipation of the next carbohydrate rich meal, secretes more insulin than you require, your blood sugar will drop. This can lead to light-headedness, headaches, irritability, and extreme hunger. This leads you to seek out a carbohydrate rich meal, drink, or snack. Although the crisis is temporarily averted and you feel better, the cycle of blood sugar instability and increased resting insulin levels has been reinforced.
Assuming you are able to reduce your caloric intake to a level below what you expend in a given day, you would expect to lose weight. As I discussed previously, it is not quite that simple. Elevated insulin inactivates the enzyme necessary to mobilize stored body fat to use it for energy. So even when you eat smaller meals, or even skip meals, if your body is so used to eating a steady supply of carbohydrates and has elevated insulin levels as a result, you will not be able to burn your body fat for energy.
Although we have been led to believe that whole grains are healthy, the statistics show the opposite. We have seen constantly increasing levels of obesity, diabetes, heart disease, and dementia as people have been encouraged to consume more grains.
Lets keep step one simple. Refined carbohydrates dump a huge amount of sugar into your body. Your body responds by burning some as energy, storing the excess as fat. Continuing this process makes burning body fat for energy very difficult.
Unfortunately it is not just candy and desserts I am referring to. Bread, cereal, pasta, low-fat sweetened yogurt, rice, soy milk, fruit, and potatoes are all carbohydrates.
To initiate weight-loss we need to change our biochemistry. Our body will respond to the fuel we supply it. If we constantly supply it with carbohydrates, it will respond as I outlined above, leaving you hungry, and making sustained weight-loss nearly impossible.
I recommend eliminating all carbohydrates except those found in non-starchy vegetables as the first step to sustainable weight-loss. This will provide the added benefits I discussed previously including: no cravings, better mood, improved mental alertness, and improved physical stamina. There are a variety of potential longer-term benefits I plan on discussing in the future as well.
A few important points:
1- When beginning a low-carbohydrate diet, your body will excrete water and salt. Please drink plenty of water, and feel free to add additional salt to your meals, especially if you feel a bit light-headed. This issue generally resolves within a few weeks.
2- You may find yourself eating because it is time to eat, rather than because you are hungry. This happened to me very quickly. It is ok to skip a meal if you are not hungry. Listen to your body, it is amazing how quickly your physiology will adapt to your new diet.
3- If you become hungry, or experience cravings for carbohydrates, eat. But do not eat carbohydrates. Eat fat. Add butter to your vegetables, use heavy cream in your coffee, eat bacon, but do not eat sugar or starches. You are teaching your body to burn fat. So you need to supply it with fat to burn. You may be surprised how quickly the carbohydrate cravings stop.
4- Do not count calories or restrict portion sizes. Just skip the carbohydrates and listen to your body.
5- Eat plenty of non-starchy vegetables and high-quality meats.
Stay tuned for the next posting where I will discuss appropriate protein levels.
I know. I just violated the first rule of weight loss. For decades, we've been told losing weight is as simple as eating less and exercising more. Everyone "knows" this is true. And we all feel bad because we have no willpower and we fail.
This idea is based on the faulty equation: (calories in) - (calories out) = change in body weight. Although thermodynamically it makes sense, biologically it doesn't always. As it turns out, this equation is a gross over-simplification of how our body works. Our bodies have not evolved to shed weight easily.
In addition to pushing highly processed, carbohydrate dense foods, our culture has suggested that we need to spend hours each week on machines doing "cardio" to maintain a healthy body weight. Since most people already do their best to follow the faulty USDA food pyramid, they often focus on lack of exercise to explain their inability to lose weight.
When I gently bring up the idea of losing weight with my patients, almost universally I hear, "I know, I need to get back in the gym..."
Not only do I think exercise as a means to lose weight is unnecessary, particularly in my orthopedic patients, it will very likely be harmful. To take a joint which has been damaged by osteoarthritis and subject it to additional, repetitive, potentially high-impact activity will very likely worsen the symptoms and accelerate the degeneration.
And yet because the large lower extremity joints (hip and knee) experience forces of 3-5 times body weight with every move they make, weight loss can be helpful in reducing pain due to arthritis. Additionally, obesity is an independent risk factor for infection following orthopedic surgery. Worse yet, poorly controlled diabetes has a synergistically negative effect with obesity on infection. Clearly, weight loss is needed. Exercise is not the way to achieve it, however.
My previous posting began to explain how WHAT we eat may be more important than how MUCH we eat. My spontaneous 25 pound weight loss occurred without entering the gym once. As an orthopedic surgeon, I am on my feet all day in the office and in the operating room, and although I consider myself "active", I did not change my activity level at all during my nutritional experiment.
Lets look at the caloric implications of exercise for a moment. A pound of body fat contains 3500 calories of energy. An average person would burn about 500 calories during an hour of jogging. Assuming you could jog for an hour every day of the week, this level of exercise would burn about 3500 calories of fat by the end of the week. If this level of activity were maintained for an entire year, about 50 pounds of body fat would "melt away." Simple. Except for a few biological problems: Appetite is not constant. Basal metabolic rate (the amount of energy you burn at rest) is not constant. Not even highly trained athletes can sustain daily exercise with no rest days and not become injured. And lastly, exercise creates inflammation, which is linked to weight GAIN, and chronic disease.
There is excellent experimental evidence suggesting an increase in appetite and calorie consumption following exercise. The sense of entitlement that often accompanies physical exertion, can undermine proper food selection, because after all, you earned that dessert by running those 5 miles this afternoon. Studies have shown a reduction in basal metabolic rate as well as reduction in non-exercise activity thermogenesis (fidgeting) when energy expenditure exceeds intake. Cardiovascular exercise fueled by carbohydrates generates oxidative stress as sugars are converted to energy in our mitochondria. Additionally, stress hormones like cortisol can be released in response to exercise, and through a variety of pathways cause weight gain. Remember our brains evolved when food was not abundant. If our energy output exceeded intake for long we would not survive. We evolved to conserve energy, and to seek out calories. This probably worked very well historically when food was scarce but has become counterproductive in the modern world where highly processed, palatable, energy dense food is omnipresent. These concepts are further developed and supported in "The Calorie Myth" by Jonathan Bailor.
Please understand that I am not recommending becoming sedentary. I am simply suggesting that we think differently about attempting to use exercise as a means to lose body fat. I recommend remaining active. Take the stairs. Don't look for the closest parking spot. Walk around the block instead of watching TV.
If you really want to lose body fat, I recommend you focus entirely on your diet. I recommend a nutrient dense, low carbohydrate, high fat diet. This does not require calorie counting. You should not feel intense cravings or blood sugar instability. Consider this a longterm/permanent lifestyle change as opposed to a diet- which generally suggests temporary, unpleasant restrictions.
Future postings will explain why I believe this way of eating helps people to lose weight, and why even those who don't need to lose weight should do it anyway. I will also explain how exactly to transition to a well-formulated low carbohydrate, high fat diet, and what you may experience while doing so.
At first glance, it may seem strange for an orthopedic surgeon to be interested in diet. Let me explain how I got here.
Throughout my life I "knew" that fat was bad, whole grains were good, and when people were overweight it was because they ate too much and exercised too little. Simple. Like many people, I did my best to keep a low fat, high carbohydrate diet. I felt guilty when I ate steak, bacon, and ice cream. When I was hungry between meals, I would often snack on pretzels because they contained no fat. When I was thirsty, I would often choose 100% fruit juice.
I remember hearing about the Atkins diet while I was in medical school. This was a diet that involved limiting carbohydrate intake and eating mostly fat. It sounded completely ridiculous to us at the time. Everyone knew that a high fat, low carbohydrate diet was clearly dangerous. I recall a biochemistry lab session where we "proved" eating in such a way offered no metabolic advantage with regard to weight-loss. The explanation was that the diet was so disgusting that people were repulsed by the fat they had to eat and therefore simply ate less.
As a practicing orthopedic surgeon, I see patients with severe arthritis involving knees, hips and shoulders everyday. Since obesity is a risk factor for osteoarthritis of the hips and knees, many of my patients are above an ideal body weight. The knees and hips are subjected to multiple times body weight with every movement and thus losing weight can have a multiplicative effect on reducing joint pain. This is a standard first-line recommendation for joint pain. This was something that we routinely recommend, but rarely occurs.
I routinely evaluate my techniques and results in an attempt to maximize good outcomes, and minimize complications. In the course of doing this, I identified 3 major risk factors linked with orthopedic infections: obesity, diabetes and smoking. This prompted a literature search which revealed that my experience was not unique. The bad news is that a large proportion of our patients had at least one of these risk factors, many had all three. The literature suggests synergy between these factors. This means the negative effects aren't just additive, but may multiply the danger.
Based on this information, I changed my practice immediately. I discussed this information with the local primary care doctors, attempting to enlist their help to keep our patients safe. I feel that each of these risk factors is modifiable. Just as we wouldn't take a patient to the operating room for a total joint replacement if they had active pneumonia, or severe coronary artery disease, we should make every effort to improve these risk factors.
I continued to get a steady stream of patients that had one or more of these risk factors referred to me because they were "ready" for their joint replacement. I then had the challenging and unusual task of explaining that while they may be mentally prepared for surgery, but were not yet medically optimized. Needless to say, patients were often surprised to hear a surgeon talking them out of surgery. An orthopedic infection is generally a big deal, often requiring multiple operations and long-term intravenous antibiotics. Once I explained my concerns to patients, many agreed to try to improve their risk profile.
Stopping smoking can be relatively simple compared to losing weight and controlling diabetes.
We gave examples of the USDA food pyramid, recommended low calorie options, focused on appropriate serving sizes, and offered referral to nutritionists. Several patients became frustrated with me, because they were unable to lose weight. They tried to eat less and exercise more. A common theme was that exercise was impossible due to the arthritis and they could only be hungry for so long until their willpower was exhausted. Some patients decided to find another orthopedic surgeon that didn't care about their risk factors. Some patients decided to undergo bariatric surgery (sleeve gastrectomy) and lost weight rapidly, but this seemed to be an extreme measure to control weight.
One day I was discussing this information with a couple. The husband was rail thin, and his wife (who was here to discuss joint replacement) was very heavy. While explaining my concerns and discussing nutrition with this couple I had a life changing revelation. The husband explained that they both eat the same food, that his wife often ate less than he did, and that he knew that she did not snack or eat secretly because she didn't drive and he did all the food shopping. I suddenly realized something we were never taught.
Different people must process calories differently. And maybe all calories are not equal?
I began researching alternatives to the standard American diet. I came across a very interesting book. "The Big Fat Surprise" by Nina Teicholz. This book alleged that all of what I knew about nutrition, despite my training as a physiology major in college, and medical school was wrong. This prompted me to read yet another book. "Good Calories, Bad Calories" by Gary Taubes. I couldn't get enough. I came across a podcast "Bulletproof Radio" by Dave Asprey. Self-described as a "bio-hacker" this network security expert managed to lose over 100 pounds and keep it off eating a high-calorie, high-fat diet. Since then I have read many thousands of pages and listened to hundreds of hours on diet, nutrition, biochemistry, and exercise. The recurrent message was that carbohydrates aren't as healthy as we think and fat isn't necessarily dangerous. Our modern diet has progressively emphasized processed carbohydrates and excluded dietary fats. While the evidence suggests that Americans are indeed following the recommendations, our difficulty with obesity, diabetes, heart disease, and dementia continues to worsen.
I never had a weight problem. Like most people I had gained a bit of weight since high school, but appeared fit. Nevertheless, I decided to do an experiment on myself. I began a high-fat, low carbohydrate diet. Just like the diet we discredited in medical school. My plan was to try this for 2 weeks. The changes were immediate. I felt much better. I lost 10 pounds and my pants were loose. I decided to extend the experiment for another month. I was so amazed at the results it is now 2 years later and I continue to eat this way. I lost a total of 25 pounds. My waistline shrunk by 3 inches. My body fat percentage is now 10%.
This was awesome, but it gets much better:
I was always mildly hypertensive (high blood pressure), and I had an occasional migraine. By the end of my first 2 week experiment, my blood pressure was perfectly normal. I have not had another migraine since the week before changing my diet. I still have a "type A" personality, but my colleagues have noticed that I am much more relaxed. I have noticed improved mental sharpness, and physical stamina.
Although this experiment was started in secret, the results were immediately obvious to friends, family members, and colleagues. Once I finished reassuring everyone that I was not ill, I then had to explain how dramatically reducing my carbohydrate intake and increasing my fat intake was responsible for my dramatic weight loss.
Even more amazing, is that my weight loss occurred rapidly and without hunger.
I believe there is mounting evidence that the long-term consumption of processed carbohydrates and exclusion of dietary fats is responsible for most of the health problems in western society. Subsequent blog postings will further develop these concepts.