Which ring do you reside?

Which ring do you reside?


Do we need say more!
Need we say more!


Terrace of the sloth: Virgil on principles of love and free will, penance of slothful` Creator: Botticelli, Sandro Date: c.1480-c.1495 


Secular Saint of The Medieval Mind and author of “The Divine Comedy,” Saint Dante Alighieri


Our Secular Patron Saint of Journalistic Writing Saint H. L. Mencken



What does Dante’s inferno will have to do with a health for fatties and fatsoes column? Let us think dear readers, gluttony, and sloth are disordered orientations of the human condition. These two orientations lead us to become fat, sloppy, lazy slugabeds and layabouts. Engaging in these deleterious habits will only lead to physical ruination. Would you like a heart bypass the age of 40? Alternatively, a bed that does absolutely everything for you with the only caveat that you cannot get out of bed; this is not a life. It is truly time to think soberly about this if you are in a 3X or larger. In addition, what about lung capacity; one does need to breath. Do you find yourself short of breath just walking up or down the house stairs or pushing the gas lawn mower one swath across your lawn? If your answer is yes to either, of the above, you are seriously in store for an enlarged heart and oxygen tank to supply pure oxygen making up for the inability to take in a sufficient quantity of air; related to the restriction of the diaphragm to expand fully because of the fatty organs pressing against it.


The Captain believes that you the reader will benefit from reading these articles in their entirety. The Captain shall dispel misinformation that is frequently disseminated by many in the MFP community. We must always remain vigilant ‘peruigil’!

The Good Captain found the following two articles of especial  interest. He is giddy with wild excitement to pass them on. The first topic below explains what are ketosis and the process of ketosis. There have been many questions concerning ketosis From the MFP members so here in all its Glory is the proper explanation.

The second article deals with restricted calorie counts and the health benefits derived from taking such an approach.   The Captain believes that you the reader will benefit from reading these articles in their entirety. The captain hopes to dispel misinformation that is frequently disseminated in the MFP. We must always remain vigilant ‘peruigil’!  




The energetic requirements of a body are composed of the basal metabolic rate and the physical activity level. This caloric requirement can be met with protein, fat, carbohydrates, or a mixture of them. Glucose is the general metabolic fuel, which can be metabolized by any cell. Fructose and some other nutrients can only be metabolized in the liver, where their metabolites are transformed either into glucose and stored as glycogen, both in the liver and in the muscles; or into fatty acids which are stored in adipose tissue.   Because of the blood–brain barrier, getting nutrients to the human brain is especially dependent on molecules that can pass this barrier. The brain itself consumes about 18% of the basal metabolic rate: on a total intake of 1800 kcal/day, this equates to 324 kcal, or about 80 g of glucose. About 25% of total body glucose consumption occurs in the brain.   Glucose can be obtained directly from dietary sugars and by the breakdown of other carbohydrates. In the absence of dietary sugars and carbohydrates, glucose is obtained from the breakdown of stored glycogen. Glycogen is a readily accessible storage form of glucose, stored in notable quantities in the liver and in small quantities in the muscles. The body’s glycogen reserve is enough to provide glucose for about 24 hours. [citation needed]   When the glycogen reserve is depleted, glucose can be obtained from the breakdown of fats from adipose tissue. Fats are broken down into glycerol and free fatty acids, with the glycerol being utilized in the liver as a substrate for gluconeogenesis.   When even the glycerol reserves are depleted, or sooner, the liver will start producing ketone bodies. Ketone bodies are short-chain derivatives of fatty acids, which, since they are capable of crossing the blood–brain barrier, can be used by the brain as an alternative metabolic fuel. Fatty acids can be used directly as an energy source by most tissues in the body.   Timeline After the exhaustion of the glycogen reserve, and for the next 2–3 days, fatty acids are the principal metabolic fuel. At first, the brain continues to use glucose, because, if a non-brain tissue is using fatty acids as its metabolic fuel, the use of glucose in the same tissue is switched off. Thus, when fatty acids are being broken down for energy, all of the remaining glucose is made available for use by the brain.   After 2 or 3 days of fasting, the liver begins to synthesize ketone bodies from precursors obtained from fatty acid breakdown. The brain uses these ketone bodies as fuel, thus cutting its requirement for glucose. After fasting for 3 days, the brain gets 30% of its energy from ketone bodies. After 40 days, this goes up to 75%. [6]   Thus, the production of ketone bodies cuts the brain’s glucose requirement from 80 g per day to about 30 g per day. Of the remaining 30 g requirement, 20 g per day can be produced by the liver from glycerol (itself a product of fat breakdown). However, this still leaves a deficit of about 10 g of glucose per day that must be supplied from some other source. This other source will be the body’s own proteins.   After several days of fasting, all cells in the body begin to break down protein. This releases amino acids into the bloodstream, which can be converted into glucose by the liver. Since much of our muscle mass is protein, this phenomenon is responsible for the wasting away of muscle mass seen in starvation.   However, the body is able to selectively decide which cells will break down protein and which will not. About 2–3 g of protein has to be broken down to synthesize 1 g of glucose; about 20–30 g of protein is broken down each day to make 10 g of glucose to keep the brain alive. However, this number may decrease the longer the fasting period is continued in order to conserve protein.   Starvation ensues when the fat reserves are completely exhausted and protein is the only fuel source available to the body. Thus, after periods of starvation, the loss of body protein affects the function of important organs, and death results, even if there are still fat reserves left unused. (In a leaner person, the fat reserves are depleted earlier, the protein depletion occurs sooner, and therefore death occurs sooner.)   The ultimate cause of death is, in general, cardiac arrhythmia or cardiac arrest brought on by tissue degradation and electrolyte imbalances.   Timeline 0 hours: Glucose still used as primary fuel.   0 – 6 hours: Glycogen is broken down to produce glucose for the body.   6 – 72 hours: Glycogen stores are used up and the body breaks down fatty acids. Ketone bodies are produced as energy for the brain.   The body’s rate of protein loss is greatest during the first 72 hours. After several days of starvation, the body adapts and starts to conserve protein. [7]   Biochemistry The human starvation response is unique among animals in that human brains do not require the ingestion of glucose to function. During starvation, less than half the energy used by the brain comes from metabolized glucose. Because the human brain can use ketone bodies as major fuel sources, the body is not forced to break down skeletal muscles at a high rate, thereby maintaining both cognitive function and mobility for up to several weeks. This response is extremely important in human evolution and allowed for humans to continue to find food effectively even in the face of prolonged starvation. [8]   Initially, the level of insulin in circulation drops and the levels of glucagon, epinephrine, and norepinephrine rise. [9] At this time, there is an up-regulation of glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis. The body’s glycogen stores are consumed in about 24 hours. In a normal 70 kg adult, only about 8,000 kilojoules of glycogen are stored in the body (mostly in the striated muscles).The body also engages in gluconeogenesis in order to convert glycerol and glucogenic amino acids into glucose for metabolism. Another adaptation is the Cori cycle, which involves shuttling lipid-derived energy in glucose to peripheral glycolytic tissues, which in turn send the lactate back to the liver for resynthesis to glucose. Because of these processes, blood glucose levels will remain relatively stable during prolonged starvation.   However, the main source of energy during prolonged starvation is derived from triglycerides. Compared to the 8,000 kilojoules of stored glycogen, lipid fuels are much richer in energy content, and a 70 kg adult will store over 400,000 kilojoules of triglycerides (mostly in adipose tissue).[10] Triglycerides are broken down to fatty acids via lipolysis. Epinephrine precipitates lipolysis by activating protein kinase A, which phosphorylates hormone sensitive lipase (HSL) and perilipin. These enzymes, along with CGI-58 and adipose triglyeride lipase (ATGL), complex at the surface of lipid droplets. The concerted action of ATGL and HSL liberates the first two fatty acids. Cellular monoacylglycerol lipase (MGL) liberates the final fatty acid. The remaining glycerol enters gluconeogenesis. [11]   Fatty acids by themselves cannot be used as a direct fuel source. They must first undergo beta-oxidation in the mitochondria (mostly of skeletal muscle, cardiac muscle, and liver cells). Fatty acids are transported into the mitochondria as an acyl-carnitine via the action of the enzyme CAT-1. This step controls the metabolic flux of beta-oxidation. The resulting acetyl-CoA enters the TCA cycle and undergoes oxidative phosphorylation to produce ATP. Some of this ATP is invested in gluconeogenesis in order to produce more glucose. [12]   Triglycerides and long-chain fatty acids are too hydrophobic to cross into brain cells, so the liver must convert them into short-chain fatty acids and ketone bodies through ketogenesis. The resulting ketone bodies, acetoacetate and β-hydroxybutyrate, are amphipathic and can be transported into the brain (and muscles) and broken down into acetyl-CoA for use in the TCA cycle. Acetoacetate breaks down spontaneously into acetone, and the acetone is released through the urine and lungs to produce the “acetone breath” that accompanies prolonged fasting. The brain also uses glucose during starvation, but most of the body’s glucose is allocated to the skeletal muscles and red blood cells. The cost of the brain using too much glucose is muscle loss. If the brain and muscles relied entirely on glucose, the body would lose 50% of its nitrogen content in 8–10 days. [13]   After prolonged fasting, the body begins to degrade its own skeletal muscle. In order to keep the brain functioning, gluconeogenesis will continue to generate glucose, but glucogenic amino acids, primarily alanine, are required. These come from the skeletal muscle. Late in starvation, when blood ketone levels reach 5-7 mM, ketone use in the brain rises, while ketone use in muscles drops.[14]   Autophagy then occurs at an accelerated rate. In autophagy, cells will cannibalize critical molecules to produce amino acids for gluconeogenesis. This process distorts the structure of the cells, and a common cause of death in starvation is due to diaphragm failure from prolonged autophagy. [15]

  1. ^Adapted from Wang et al. 2006, p 223.
  2. ^Dieting and Metabolism
  3. ^Therapeutic Fasting
  4. Ask an Expert: Fasting and starvation mode^
  5. ^
  6. ^ J. Coffee, Quick Look: Metabolism, Hayes Barton Press, Dec 1, 2004, p.169
  7. ^http://www.ncbi.nlm.nih.gov/pubmed/9665093
  8. ^Cahill, GF and Veech, RL (2003) Ketoacids? Good Medicine?, Trans Am Clin Clim Assoc, 114, 149-163.
  9. ^Zauner, C., Schneeweiss, B., Kranz, A., Madl, C., Ratheiser, K., Kramer, L., … & Lenz, K. (2000). Resting energy expenditure in short-term starvation is increased because of an increase in serum norepinephrine. The American journal of clinical nutrition, 71(6), 1511-1515.
  10. ^Clark, Nancy. Nancy Clark’s Sports Nutrition Guidebook. Champaign, IL: Human Kinetics, 2008. pg. 111
  11. ^
  12. ^Zechner, R, Kienesberger, PC, Haemmerle, G, Zimmermann, R and Lass, A (2009) Adipose triglyceride lipase and the lipolytic catabolism of cellular fat stores, J Lipid Res, 50, 3-21
  13. ^McCue, MD (2010) Starvation physiology: reviewing the different strategies animals use to survive a common challenge, Comp Biochem Physiol, 156, 1-18
  14. ^
  15. ^




Effects on humans

Positive effects Biomarkers for cardiovascular risk In 2004, Fontana et al. published data from a study of 18 individuals who had been on CR for an average of 6 years and 18 age-matched healthy individuals on typical American diets. The study took one set of measurements of risk factors for atherosclerosis from each group and compared them and found that “it appears that long-term CR has a powerful protective effect against atherosclerosis.”[11] The study noted that the high quality diets consumed by the CR practitioners may be responsible for some of these beneficial effects.[11]   Data from the NIA-funded CALERIE phase 1 randomized clinical trials show that 20% CR for 12 months in overweight individuals results in a significant reduction in visceral fat mass, LDL-cholesterol, triglycerides, and C-reactive protein, and improves insulin sensitivity.[12]   Biomarkers for cancer risk Long-term CR in humans results in a reduction of several metabolic and hormonal factors that have been associated with increased risk of some of the most common types of cancer in developed countries.[13] Individuals practicing CR without malnutrition have lower levels of total and abdominal fat, circulating insulin, testosterone, estradiol and inflammatory citokines.[14][15][16] However, unlike in rodents, long-term CR does not reduce serum IGF-1 levels in humans, unless protein intake is also reduced.[17][18]   Negative effects The long-term effects of moderate CR with adequate intake of nutrients on humans are still unknown.[19] However, severe or extreme CR may result in serious deleterious effects, as it has been shown in the “Minnesota Starvation Experiment”.[20] This study was conducted during World War II on a group of lean men, who restricted their calorie intake by 45% for 6 months.[20] As expected, this severe degree of CR resulted in many positive metabolic adaptations (e.g. decreased body fat, blood pressure, improved lipid profile, low serum T3 concentration, and decreased resting heart rate and whole-body resting energy expenditure), but also caused a wide range of negative effects, such as anemia, lower extremity edema, muscle wasting, weakness, neurological deficits, dizziness, irritability, lethargy, and depression.[20]   Musculoskeletal losses Short-term studies in humans report loss of muscle mass and strength and reduced bone mineral density.[21] This is to be expected as part of the weight loss that accompanies CR. Beyond using lean tissue as an energy source, the presence of catabolic hormones, such as cortisol, and the lack of anabolic ones, such as insulin, disrupts protein synthesis, amino acid uptake, and immune response.   People who lose weight as a result of CR but who are sedentary have a reduced capacity to perform exercise compared with those who lost similar amounts of weight from exercise alone,[22] emphasizing the need for strength training in CR practitioners.   A study of long-term CR practitioners “who had been eating a CR diet (approximately 35% less calories than controls) for an average of 6.8 ± 5.2 years (mean age 52.7 ± 10.3 years)” found that they had reduced bone mineral density at the level of hip and spine, in accordance with a previous one-year weight-loss trial,[23] but that after initial weight loss they had achieved a stable, normal level of bone turnover and that the micro architectural structure of their bones was healthy; the researchers concluded that “These findings suggest that markedly reduced BMD is not associated with significantly reduced bone quality in middle-aged men and women practicing long-term calorie restriction with adequate nutrition.”[24] Some specialists say that minor mineral losses can be minimized with regular physical activity and vitamin D and calcium supplements.[25]   Similarly, despite acute reductions in muscle mass at onset, CR retards the age-related loss of muscle structure and function (sarcopenia) in nonhuman primates[26][27] and rodents;[28][29] however, no longitudinal data are available on this subject in humans.   The authors of a 2007 review of the CR literature warned that “[i]t is possible that even moderate calorie restriction may be harmful in specific patient populations, such as lean persons who have minimal amounts of body fat.”[30]   Low BMI, high mortality CR diets typically lead to reduced body weight, and in some studies, low body weight has been associated with increased mortality, particularly in late middle-aged or elderly subjects. One of the more famous of such studies linked a body mass index (BMI) lower than 18 in women with increased mortality from noncancer, non−cardiovascular disease causes.[31] The authors attempted to adjust for confounding factors (cigarette smoking, failure to exclude pre-existing disease); others argued that the adjustments were inadequate.[32]   “epidemiologists from the ACS (American Cancer Society), American Heart Association, Harvard School of Public Health, and other organizations raised specific methodologic questions about the recent Centers for Disease Control and Prevention (CDC) study and presented analyses of other data sets. The main concern … is that it did not adequately account for weight loss from serious illnesses such as cancer and heart disease … [and] failed to account adequately for the effect of smoking on weight … As a result, the Flegal study underestimated the risks from obesity and overestimated the risks of leanness.”[33] While low body weight in the elderly can be caused by conditions associated with aging (such as cancer, chronic obstructive pulmonary disorder, or depression) or of the cachexia (wasting syndrome) and sarcopenia (loss of muscle mass, structure, and function),[34] the results of a large epidemiological study published in the fall of 2011 show that among the Japanese, an association between a BMI under 21 (under 65 kg for a 1.75 m tall individual (or in imperial units, under 140 lb. for a 5′-9” tall individual)) and increased mortality persists even when confounders like age, smoking, and disease are carefully controlled for.[35]   Such epidemiological studies of body weight are not about CR as used in anti-aging studies; they are not about caloric intake to begin with, as body weight is influenced by many factors other than energy intake. Moreover, “the quality of the diets consumed by the low-BMI individuals are difficult to assess, and may lack nutrients important to longevity.” [19] Typical low-calorie diets rarely provide the high nutrient intakes that are a necessary feature of an anti-aging calorie restriction diet.[36][37][38] As well, “The lower-weight individuals in the studies are not CR because their caloric intake reflects their individual ad libitum set-points, and not a reduction from that set-point.” [19]   Triggering eating disorders Concerns are sometimes raised that CR can make people feel hungry all the time and may lead to obsessing about food, causing eating disorders.[22] However, a controlled study of human CR found no increase in eating disorder symptoms or other harmful psychological effects, in line with extensive earlier research.[39] In those who already suffer from a binge-eating disorder, calorie restriction can precipitate an episode of binge eating, but it does not seem to pose any such risk otherwise.[40]   Not for the young or those seeking to become pregnant Long-term calorie restriction at a level sufficient for slowing the aging process is generally not recommended in children, adolescents, and young adults (under the age of approximately 21), because this type of diet may interfere with natural physical growth, as has been observed in laboratory animals. In addition, mental development and physical changes to the brain take place in late adolescence and early adulthood that could be negatively affected by severe calorie restriction.[41] Pregnant women and women trying to become pregnant are advised not to practice calorie restriction, because low BMI may result in ovulatory dysfunction (infertility), and underweight mothers are more prone to preterm delivery.[41]   Miscellaneous concerns It has also been noted that people losing weight on such diets risk developing cold sensitivity, menstrual irregularities, and even infertility and hormonal changes.[42]   Moreover, calorie restriction has been reported in mice to hinder their ability to fight infection, and some evidence suggests that in patients with amyotrophic lateral sclerosis, calorie restriction accelerates the onset of the disease.[43]   Excessive calorie restriction may result in starvation.   Effects of CR on life span in different organisms Primates A study on rhesus macaques funded by the National Institute on Aging was started in 1989 at the University of Wisconsin–Madison and is still ongoing. Monkeys were enrolled in the study at ages of between 7 and 14 years. Preliminary results published in 2000 showed lower fasting insulin and glucose levels as well as higher insulin sensitivity and LDL profiles, associated with lower risk of atherogenesis in dietary-restricted animals.[44] CR also attenuated age-related loss of muscle mass and function (sarcopenia) in these primates.[26][27] Results published in 2009 showed that caloric restriction in rhesus monkeys blunts aging and significantly delays the onset of age-related disorders such as cancer, diabetes, cardiovascular disease, and brain atrophy. 80% of the calorie-restricted monkeys were still alive, compared to only half of the controls.[45] [46] Results to date have also found a trend toward a reduced overall death rate, which has not yet reached statistical significance. An additional analysis, restricted to causes of death related to aging, did find a significant reduction in age-related deaths. However, the interpretation of this finding is uncertain, as it is hypothetically possible that the exclusion of deaths due to non-aging causes may somehow mask an involvement of CR in such deaths, although the sample size is too low to say for certain.[1][3] A study published in 2011 examined the effect of stress on various brain functions in these monkeys.[47] In the control group, stress reactivity was associated with less volume and tissue density in areas important for emotional regulation and the endocrine axis, including prefrontal cortices, hippocampus, amygdala, and hypothalamus. CR reduced these relationships.   In contrast to the conclusions reached by the University of Wisconsin–Madison (WNPRC) study, a 2012 National Institute on Aging (NIA) study published in the journal Nature, concluded that a calorie restriction regimen did not improve survival outcomes whether implemented in young or older age rhesus monkeys.[48] A key difference between the WNPRC and the NIA studies is that the monkeys in the WNPRC study were fed a more unhealthy diet.[49]   In 2006, researchers at New York’s Mount Sinai School of Medicine reported results comparing the brains of 3 monkeys fed a normal diet and 3 monkeys on a CR diet for their entire lives. The normal diet group “consisted of three male Squirrel monkeys (20–27 years old), who died from congestive heart failure, liver failure or complications of intestinal bleeding, respectively; the weight at the time of death of the CON group ranged 526–866 g. The CR group consisted of 3 male Squirrel monkeys (15–20 years old) on CR diet for 14 to 18 years, who died from inanition, complications of bleeding or by complications from liver necrosis, respectively; the weight at the time of death of CR group ranged 526–813.”[50] The squirrel monkeys on a lifelong calorie-restrictive diet were less likely to develop Alzheimer’s-like changes in their brains.[50] Notes

  1. ^ ab c d e
  2. ^
  3. ab c
  4. ^
  5. ^
  6. ^The Anti-Aging Plan: Strategies and Recipes for Extending Your Healthy Years by Roy Walford (page 26)
  7. ^Cava E et al. humans? Aging (Albany NY).2013 Jul;5(7):507-14.
  8. ^Rickman AD et al. The CALERIE Study: Design and methods of an innovative 25% caloric restriction interventionContemp Clin Trials. 2011 November; 32(6): 874–881.
  9. ^
  10. ^
  11. ab
  12. ^Fontana L, et al. Calorie restriction or exercise: effects on coronary heart disease risk factors. A randomized, controlled trial. Am J Physiol Endocrinol Metab. 2007 Jul;293(1):E197-202
  13. ^Calle EE, Kaaks R. Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms. Nat Rev Cancer. 2004 Aug;4(8):579-91
  14. ^Cangemi R, Friedmann AJ, Holloszy JO, Fontana L. Long-term effects of calorie restriction on serum sex-hormone concentrations in men. Aging Cell. 2010 Apr;9(2):236-42
  15. ^Fontana L, Klein S, Holloszy JO. Effects of long-term calorie restriction and endurance exercise on glucose tolerance, insulin action, and adipokine production. Age (Dordr). 2010 Mar;32(1):97-108
  16. ^Meyer TE, Kovács SJ, Ehsani AA, Klein S, Holloszy JO, Fontana L. Long-term caloric restriction ameliorates the decline in diastolic function in humans. J Am Coll Cardiol. 2006 Jan 17;47(2):398-402
  17. ^
  18. ^Redman LM, Veldhuis JD, Rood J, Smith SR, Williamson D, Ravussin E; Pennington CALERIE Team. The effect of caloric restriction interventions on growth hormone secretion in nonobese men and women. Aging Cell. 2010 Feb;9(1):32-9.
  19. ab c
  20. ab c Keys A, Brozek J, Henschels A & Mickelsen O & Taylor H. The Biology of Human Starvation, 1950, Vol. 2, p. 1133. University of Minnesota Press, Minneapolis
  21. ^
  22. ab
  23. ^
  24. ^
  25. ^http://www.turner-white.com/memberfile.php?PubCode=jcom_apr07_calcium.pdf
  26. ab c d
  27. ab c
  28. ab c
  29. ab c
  30. ^
  31. ^
  32. ^
  33. ^
  34. ^
  35. ^
  36. ^
  37. ^
  38. ^
  39. ^
  40. ^
  41. ab
  42. ^
  43. ^
  44. ^
  45. ^
  46. ab Reduced Diet Thwarts Aging, Disease In MonkeysScience Daily, July 10, 2009
  47. ^
  48. ^
  49. ^Calorie restriction falters in the long run Nature News, August 29, 2012
  50. ^ ab

“The Fat Bastard Gazette” does not purport to offer any definitive medical or pharmaceutical advice whatsoever in any explicit or implied manner. Always consult a qualified physician in all medical or pharmaceutical matters. “The Fat Bastard Gazette” is only the opinion of informed nonprofessionals for the general edification and entertainment of the greater public.  

 No similarities to any existing names or characters are expressed or implied. We reserve the right to offend or support anybody, anything, or any sacred totem across the globe.  

                                                                                                                       Cordially Yours,                                                                                                                          Captain Q.


Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s