Also see Anti-Cancer Effects of Fasting
Intermittent fasting, is where you set hours on a daily, or weekly, or monthly schedule, where you drink water, but do not consume calories. In my practice, it has nothing to do with calorie reduction, just changing the schedule of when I eat. I fast around 16 hours a day. The best way to do this is to have some purpose in your life, such that you are too distracted by that purpose to bother with eating.
There is a lot more on the internet about intermittent fasting than when I began practicing in 2012. It has grown in popularity, so there are likely to be better articles than this one, especially since I never intended to write one when I was researching back then. It's starting to be noticed by reputable institutions such as Harvard. Another mainstream article.
My schedule for intermittent fasting had varied quite a bit. I focused more on not eating for 16 hours than the 8 hour window. I would go to bed anywhere from 10pm to 3am, which is not great for the circadian rhythm. More about circadian rhythms here. A valuable piece of information I just came across:
“In humans, four pilot trials of TRF (4–10-hr feeding periods) have been conducted to date. Surprisingly, the results of TRF in humans appear to depend on the time of day of the eating window. Restricting food intake to the middle of the day (‘‘mid-day TRF’’ [mTRF]) reduced body weight or body fat, fasting glucose and insulin levels, insulin resistance, hyperlipidemia, and inflammation. However, restricting food intake to the late afternoon or evening (after 16:00 hr.; ‘‘late TRF’’) either produced mostly null results or worsened postprandial glucose levels, b cell responsiveness, blood pressure, and lipid levels.” source
What I understand of the late TRF is that they were eating between 4pm and 10pm, then sleeping an hour or so after dinner. I don't like eating when I wake, so I will opt for mid-day TRF, around 1pm-2pm to 7pm-8pm, giving myself 3 hours without eating before sleeping. I'm not sure if that's optimal, but it suits my lifestyle better. In effect I will narrow my eating window to 6 hours, where before it was around 8, where I just focused more on not eating for 16.
Update 20190318: I fasted for 9.5 days. My visceral fat is significantly reduced, and I only have an inch to pinch of subcutaneous fat on my stomach. I didn't have a weight scale, but I estimate 8 lbs lost. I'm going to continue with intermittent fasting, and not eating late (as described in the section below). I'm still not a fan of having breakfast so I'll see how things work for me. Previously my 8 hour eating window ranged between 2pm and 10pm. Fact of life is that social eating happens mostly in the evening. I'll find a healthy vs social balance.
Apart from all the benefits supported by research on fasting, one hope I have is to see long term weight loss occur in a short period of time. There would be a certain satisfaction in seeing the benefit after a week or two. I have a hypothesis that when you've increased weight, that you have permanently increased the number of fat cells you have, and that this number of fat cells does not decrease with loss of weight, and affects your body's appearance long term (for example, your belly is never completely flat again, even with a low BMI).
“ Liposuction reduces the number of fat cells in a person’s body, but studies show the weight lost is typically regained within a year. It isn’t known whether this regain occurs through the production of new fat cells or expansion of existing ones. ” https://well.blogs.nytimes.com/2017/02/17/are-fat-cells-forever
My hope is that by long term fasting, I will achieve adipocyte apoptosis (fat cell death), but I have not found any research to support this hypothesis. I haven't read all the research I've found in the last section below, as I don't want to make a huge investment in this. I decided to just try a long term fast, since from what I've read, there is benefit to be had even if I don't get the particular result of “adipocyte apoptosis with beneficial body contouring”.
Update: In mice that went through fasting and refeeding, visceral fat was consumed at a faster rate upon fasting, and upon refeeding, subcutaneous fat recharged at a faster rate.1 That's a good start, and I wish I could find more support. Even if visceral fat is the best type of fat to be losing, it would still be good to burn off love-handles. However, from this single mouse study, it appears it might be more difficult.
Increasing adipocyte apoptosis through supplements:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5459503 (Xanthene MI-401)
https://onlinelibrary.wiley.com/doi/abs/10.1002/mnfr.201300503 (Calcium and Vit D)
I'm also worried about regaining the weight, given a slower metabolism upon finishing the fast. I assume slowly increasing *healthy* food intake will help with that.
When you fast, your body enters a state called ketosis, where it burns fat as it's primary fuel source. You can enter ketosis after just 12 hours of fasting, but apparently, it's not an on/off switch. You can be in ketosis to a certain degree: “Fasting for just 12 - 16 hours can achieve ketosis, albeit at lower levels at about ~.05mM.7 But a 48-hour fast can boost ketone levels in the blood by 20x, between 1 - 2mM.”1
My previous experience with a long fast, I only drank water. After 3.5 days, although physically fit, I found myself stopping to catch my breath while trying to climb two flights of stairs. I was on my way to eat a banana. Perhaps this lack of energy was due to insufficient vitamins or relevant small molecules. People have mixed results fasting, feeling either energized or fatigued.12
Another factor that may have influenced “bonking”, is that my body was not sufficiently trained at using fat as the primary fuel source: “By following a very low carbohydrate diet, or ketogenic diet, you can train your body to burn fat. Similarly, by exercising in the fasted state, you can train your muscles to burn fat. Now, instead of relying on limited but easily accessible glycogen during competition, you are powered by an almost unlimited energy drawn directly from your fat stores.” 1 Even if I could train my body to fast by slowly increasing the number of days of each fast, I would rather see results accomplished in a single fast. However, I don't want to be so weak as to be non-functional, hence my desire to supplement.
I plan to take dietary supplements and electrolytes. Since some supplements require fat for proper absorption, I will have ~20g of fat (a few bites of food that has no more than 10g of carbs). I will also take 5gm of glucomannan fiber as I think one of its benefits is maintaining hydration, which may be a challenge while fasting. Note that with fat intake, limited protein and very limited carbs, the body will stay in ketosis.
One possible downside, is that by taking supplements, I may be avoiding a beneficial hormetic response:
DRI Daily Reference Intake includes a 2016 update to RDA. The supplements I will take are listed here, which includes a multi-vitamin. Not included in the supplements listed are electrolytes, that I usually get enough of from food. Adequate intake AI/RDA for electrolytes here and here.
Adequate Intake AI or RDA for me (since it depends on age and sex):
potassium 3500mg or 4700mg depending on who you ask
magnesium 420mg, or another source
calcium 1000mg (from google search)
Not covered by the DRI: Bicarbonate ~300mg
The big three are sodium, potassium, and magnesium (conclusion based on non-peer-reviewed research sources). According to this site Calcium… “Chloride, Phosphorus,
Phosphate, Bicarbonate, and Natrium Chloride also have a major role to play in maintaining a proper electrolyte balance in the body”. I used strike-through in the quote for phosphate, because I can't find any reference to phosphate being a nutrient, and also natrium chloride, because that's just another name for sodium chloride.
For potassium, NuSalt or NoSalt is recommended (potassium chloride).
For magnesium I take a supplement.
For calcium I may need to obtain a supplement.
For phosphorus I may need to obtain a supplement.
For sodium, this recipe: this site recommends ½ cup of water, ½ tsp of baking soda (sodium bicarbonate), 2 tsp of apple cider vinegar, and a pinch of lemon juice (optional), to obtain the necessary sodium. 1 tsp of baking soda has 1259 mg of sodium. ACV will have trace amounts of nutrients, but not enough to make a dent in the RDA.
When fasting, you need extra sodium: 4 to 7 grams according to many sites, although I haven't found any peer reviewed research that says this. Because salt is sodium chloride, the amount of salt you need is greater. One teaspoon of Himalayan salt converted to gram equals to 5.7g, which contains ~1700mg of sodium. Chemistry-wise, sodium chloride is 40% sodium and 60% chloride by weight, but Himalayan salt contains less sodium compared to table salt.
I considered that within all the herbs I take, I may be getting electrolytes that I need:
calcium: Turmeric contains 183mg calcium per 100g (18% RDA), and I supplement 1.4g. Basil contains 1684mg per 100g and I supplement holy basil at 800mg. 1
phosphorus: Turmeric contains 268mg per 100g and I supplement 1.4g. Garlic powder contains 417mg per 100g and I supplement 400mg. Ginger 148mg per 100g. Basil 56mg per 100g. 2
Maybe some of the other herbs I take probably contain electrolytes as well, but I don't think they will add up to much given the above reference of 100g. However, I do consume a small amount of food with fat, for those supplements that require fat for absorption. This includes almond butter, which is high in phosphorus and calcium.
Update: I'm in 6 days into the supplemented fast. I didn't stay on top of the recommended electrolyte intake. I've felt weak but not with the severity I experienced in a 3.5 day water-only fast. I can't conclude what favors the reduced weakness more: the 400 calories a day, the supplements, or low dosages of electrolytes, but either way I'm able to function.
The body does not prefer burning muscle for energy:
Adipocyte apoptosis is bad… what?
Other people's experiences on 400 calories a day:
Loss of White Adipose Hyperplastic Potential Is Associated with Enhanced Susceptibility to Insulin Resistance
“The adipocyte is increasingly recognized as a regulator of energy balance, systemic metabolism, and inflammation (Cristancho and Lazar, 2011). Despite the intuitive appeal of targeting adipocytes as a pathologic component of obesity, a number of often-cited observations support the concept that a dynamic adipocyte pool maybebeneficial instatesof excessenergy consumption. Stimulation of PPARg-dependent adipogenesis with thiazolidinedione drugs, for example, is associated with an insulin sensitizing effect, although distinguishing the specific effects of PPARg activation responsible for this beneficial property is an area of active research (Choi et al., 2010).”
Adipose Tissue Plasticity: How Fat Depots Respond Differently to Pathophysiological Cues
“White adipose tissue (WAT) has key metabolic and endocrine functions and plays a role in regulating energy homeostasis and insulin sensitivity. WAT is characterised by its capacity to adapt and expand in response to surplus energy through processes of adipocyte hypertrophy and/or recruitment and proliferation of precursor cells in combination with vascular and extracellular matrix remodelling. However, in the context of sustained obesity, WAT undergoes fibro-inflammation, which compromises its functionality, contributing to increased risk of type 2 diabetes and cardiovascular diseases.”
“…overeating impairs the ability of brain insulin to suppress the breakdown of fat in adipose tissue.” 1
In the following links, corresponding full articles may be found at the top right of the page
2010 / CellCycle / Fasting and differential chemotherapy protection in patients / Rafaghello, Prof. Valter Longo, et al./ DOI: 10.4161/cc.9.22.13954
2010 / Trends in Pharmacological Sciences / Calorie restriction and cancer prevention: metabolic and molecular mechanisms / Prof Valter D. Longo and Luigi Fontana / DOI: 10.1016/j.tips.2009.11.004
2007 / PNAS / Starvation‐dependent differential stress resistance protects normal but not cancer against high‐dose chemotherapy / Lizzia Raffaghello, Prof. Valter Longo, et al. / DOI: 10.1073“pnas.0708100105
2011 / Oncogene Research / Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients / Changhan Lee and Prof. Valter Longo / DOI: 10.1038/onc.2011.91
A.J.Carlson and F. Hoelzel, “Nutrition, Senescence and Rejuvenescence”. Public Health Reports Vol.67 No.2. February 1952 Chicago.
H.L.Taylor, “American Journal of Physiology”. pp143-148 1945.
A.J.Carlson and F. Hoelzel, “Apparent Prolongation of Lifespan of Rats by Intermittent Fasting”. Journal of Nutrition, 31:363 1946.
Sergius Morgulis, “Fasting and Undernutrition”. University of Nebraska, E.P. Dutton, New York 1923.
A.J.Carlson, “The Control of Hunger in Health and Disease”. University of Chicago 1916.
Margaret M. Kunde, “The After Effects of Prolonged Fasting on the Basal Metabolic Rate”. Journal of Metabolic Research 1923, 3, 399 – 449.
R.H. Weindruch, J.A.Kristie, K.Cheney and R.L.Walford, “The Influence of Controlled Dietary Restriction on Immunologic Function and Ageing”. Federation Proceedings U.C.L.A. 389:2007 (1979)
‘Caloric restriction in C57BL/6J mice mimics therapeutic fasting in humans.’ - Mahoney LB, Denny CA, Seyfried TN. Biology Department, Boston College, Chestnut Hill, MA, USA. 2006
Based on my previous knowledge, I approve of this bulletproof article in the overall strategy of reducing visceral fat: