I really enjoyed the time I spent with the whoop strap. We sadly parted ways after 19 months of 24/7 interaction. I previously discussed how much data this device provides to you. In addition to providing data, I found the whoop strap gently nudging me to make healthier choices. While the app would offer suggestions with regard to bedtime, it was never intrusive. The true power of the device is in the data it collects, summarized and then presents to you very clearly. Objective data is very powerful. It is not theoretical. It clearly shows the effects of choices you make each day. The best way to study these lifestyle choices is by using the journal function. With only a few swipes on the app, whatever behaviors you are tracking can be logged each morning. A summary of the effects of these behaviors will show up monthly in the app. This objective data will result in lifestyle improvements. 

Here is what I learned. 

​Whole, unprocessed foods lead to improved recovery. Veering off my usual low carb, high fat diet resulted in poorer recovery scores. I have written about this extensively elsewhere in this blog. 

Intermittent fasting improved my recovery scores. This reinforced what I had been doing for years and had written about earlier. 

Eating just before bed interferes with recovery, primarily by  interfering with sleep. 

Magnesium glycinate supplement improves sleep performance. This was a supplement I had been using for years. It clearly showed up

Resistance exercise (weight-lifting) does not register as much strain. (But it will reduce recovery). The whoop strap is designed primarily to track cardiovascular exercise and the recovery score represents how ready your body is for cardiovascular stress. While a very strenuous resistance exercise workout will not increase your strain for the day very much (since it will not generally create a sustained increase in heart rate), it will show up indirectly with a lower recovery than you might otherwise expect the following day. Thus, the whoop strap is not "missing" the effects of this workout as some believe by not elevating your strain score, it is absolutely registering its effects on your nervous system, and will guide you to optimize your fitness regimen based on the reduced recovery score.

I also liked the fact that the battery would last for 4-5 days and there was no need to remove the device to charge it. This allowed constant monitoring throughout the day and night. The device and the battery are both waterproof. The journal feature  is quite powerful. It allows quick and easy tracking of behaviors, and correlates them with your strain and recovery. This information is very helpful when making lifestyle choices. 

The whoop system provides lots of data. This data is presented in graphic form that allows you to rapidly identify trends. 

Because this device is only an instrument for data collection, and does not have a screen of its own, it must be used with your smart phone. Since the whoop strap will collect data and then upload to your phone in the future, you do not need to carry your phone at all times. It will sync when back within bluetooth range.  The inability to display any data is something to consider when you are shopping for fitness tracking devices. Watches are much more versatile. 

While I truly enjoyed using this device, and consider it a powerful tool, I ultimately chose to unsubscribe from the service. Why?

The subscription based service is the reason I discontinued with Whoop. The base price of this service is about a dollar per day. This is decent value for the data it provides. I originally signed up for an 18 month, discounted rate, and could have done so again. The problem is that I I really enjoyed gathering this data, tracking my activities, and monitoring my recovery/fitness levels. I would like to collect this data forever. Unfortunately, it is not currently possible to purchase a whoop device. Ongoing subscription long-term makes this device the most expensive on the market. At this time, I feel I have learned all the lessons I wanted to learn. I truly understand my body better now. This has been a very valuable experience, and I recommend it to particularly for someone training for a cardiovascular endurance event, or for anyone simply interested in improving their health/recovery. I am currently researching a similar device that I can buy once, and own forever. 

My next article will dig into the lessons I learned from whoop. 
​

Some people are reluctant to try a low carbohydrate, high fat diet as we have heard for decades that a high fat diet will cause heart disease. This is based on the so called "lipid hypothesis" which, when scrutinized, appears to have been based on very biased studies.  It does, however, appear that low triglycerides, low lipoprotein(a), low insulin resistance, and high HDL are all associated with reduced cardiovascular risk. 

A recent study: "Effects of a low-carbohydrate diet on insulin- resistant dyslipoproteinemia- a randomized controlled feeding trial," is an excellent example of how good nutritional research should be performed. Unlike most nutritional studies, it does not rely on food surveys, which are notoriously inaccurate. It is an actual interventional study.

3 groups of patients were randomized. All of their meals were prepared by the study administrators. All groups had the same 20% protein content. After an initial 10-14% weight loss which was achieved on the same run-in diet, the groups were then stratified into low-carb (20%), moderate-carb (40%), and high-carb (60%) meals. The low carb group ate 21% saturated fat, moderate carb 14% saturated fat, and low carb 7% saturated fat. 

Lipid markers associated with cardiovascular risk were tested at baseline and then at 20 weeks.

The lipid hypothesis would predict the  low carb/high saturated fat group would experience elevated cardiovascular risk. 

What was actually found? 

Exactly the opposite. The low-carbohydrate, high-fat group experienced improvement in  insulin resistance, improvement in triglyceride levels, reduced lipoprotein(a), and increased HDL and adiponectin. These all indicate improved cardiovascular risk.

​So- now we have a very well done nutritional study which suggests doing the opposite of the traditionally recommended diet (food pyramid) appears to improve cardiovascular risk factors. 

I hope we will continue to see nutritional studies performed that are as well designed as this one. 

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. 

INSULIN RESISTANCE
​
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:

Weight loss
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.

Insulin Sensitivity
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. 

Cardio-protective
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.

Neuro-Protective
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.

Mental Health
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.  

Anti-inflammatory
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. 

​Anti-cancer
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. 

Radiation Protective
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. 


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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.
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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.
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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.

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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.

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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. 

In summary:

1. Do not fear dietary fat.
2. Track your cardiovascular risk factors (HDL, triglycerides, body weight, waist circumference.)
3. Cook with saturated fats.
4. Choose unprocessed, undamaged unsaturated fats.
5. Do not cook with  unsaturated fats.
6. Increase wild caught seafood consumption to improve omega 3 intake.
7. Reduce vegetable oil consumption to reduce omega 6 intake.

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.