low-carbohydrate diets

[Jhanananda]

Ever since I was diagnosed with diabetes about 3 years ago, I have been attempting to live on a low-carbohydrate diet.  It has taken me almost the whole time to learn what a low-carbohydrate diet is.  It has succeeded in reducing my fasting blood sugar level by about 50 points, which was not enough; however, it is reasonable to consider that a low-carbohydrate diet should be the base of anything else one does to control blood sugar.

It is interesting to note that the definition of a low-carbohydrate diet in wikipedia includes eggs, which are low in carbs and high in chromium; nonetheless recent research posted elsewhere here under chromium & diabetes has shown that eggs raise the blood sugar significantly; however, I have not found that to be true in my case.

Low-carbohydrate diets or low-carb diets are dietary programs that restrict carbohydrate consumption, often for the treatment of obesity or diabetes. Foods high in easily digestible carbohydrates (e.g., sugar, bread, pasta) are limited or replaced with foods containing a higher percentage of fats and moderate protein (e.g., meat, poultry, fish, shellfish, eggs, cheese, nuts, and seeds) and other foods low in carbohydrates (e.g., most salad vegetables), although other vegetables and fruits (especially berries) are often allowed. The amount of carbohydrate allowed varies with different low-carbohydrate diets.

Such diets are sometimes 'ketogenic' (i.e., they restrict carbohydrate intake sufficiently to cause ketosis). The induction phase of the Atkins diet[1][2][3] is ketogenic.

The term "low-carbohydrate diet" is generally applied to diets that restrict carbohydrates to less than 20% of caloric intake, but can also refer to diets that simply restrict or limit carbohydrates to less than recommended proportions (generally less than 45% of total energy coming from carbohydrates).[4][5]

Low-carbohydrate diets are used to treat or prevent some chronic diseases and conditions, including cardiovascular disease, metabolic syndrome, high blood pressure, and diabetes.[6][7]

Prehistory
See also: Paleolithic: Diet and nutrition

As with the Paleolithic diet, several advocates of low-carbohydrate diets have argued that these diets are closer to the ancestral diet of humans before the origin of agriculture, and humans are genetically adapted to diets low in carbohydrate.[8] Direct archaeological or fossil evidence on nutrition during the Paleolithic, when all humans subsisted by hunting and gathering, is limited, but suggests humans evolved from the vegetarian diets common to other great apes to one with a greater level of meat-eating.[9] Some close relatives of modern Homo sapiens, such as the Neanderthals, appear to have been almost exclusively carnivorous.[10]

A more detailed picture of early human diets before the origin of agriculture may be obtained by analogy to contemporary hunter-gatherers. According to one survey of these societies, a relatively low carbohydrate (22–40% of total energy), animal food-centered diet is preferred "whenever and wherever it [is] ecologically possible", and where plant foods do predominate, carbohydrate consumption remains low because wild plants are much lower in carbohydrate and higher in fiber than modern domesticated crops.[11] Primatologist Katherine Milton, however, has argued that the survey data on which this conclusion is based inflate the animal content of typical hunter-gatherer diets; much of it was based on early ethnography, which may have overlooked the role of women in gathering plant foods.[12] She has also highlighted the diversity of both ancestral and contemporary foraging diets, arguing no evidence indicates humans are especially adapted to a single paleolithic diet over and above the vegetarian diets characteristic of the last 30 million years of primate evolution.[13]

The origin of agriculture brought about a rise in carbohydrate levels in human diets.[14] The industrial age has seen a particularly steep rise in refined carbohydrate levels in Western societies, as well as urban societies in Asian countries, such as India, China, and Japan, with resulting increases in obesity rates.
Early dietary science

In 1797, John Rollo reported on the results of treating two diabetic Army officers with a low-carbohydrate diet and medications. A very low-carbohydrate, ketogenic diet was the standard treatment for diabetes throughout the 19th century.[15][16]

In 1863, William Banting, a formerly obese English undertaker and coffin maker, published "Letter on Corpulence Addressed to the Public", in which he described a diet for weight control giving up bread, butter, milk, sugar, beer, and potatoes.[17] His booklet was widely read, so much so that some people used the term "Banting" for the activity usually called "dieting".[18]

In 1888, James Salisbury introduced the Salisbury steak as part of his high-meat diet, which limited vegetables, fruit, starches, and fats to one-third of the diet.[original research?]
Modern low-carbohydrate diets

In 1958, Richard Mackarness M.D. published Eat Fat and Grow Slim, a low-carbohydrate diet with much of the same advice and based on the same theories as the Atkins diet. Mackarness also challenged the "calorie theory" and referenced primitive diets such as the Inuit as examples of healthy diets with a low-carbohydrate and high-fat composition.

In 1967, Irwin Stillman published The Doctor's Quick Weight Loss Diet. The "Stillman diet" is a high-protein, low-carbohydrate, and low-fat diet. It is regarded as one of the first low-carbohydrate diets to become popular in the United States.[19] Other low-carbohydrate diets in the 1960s included the Air Force diet[20] and the drinking man’s diet.[21] Austrian physician Wolfgang Lutz published his book Leben Ohne Brot (Life Without Bread) in 1967.[22] However, it was not well known in the English-speaking world.

In 1972, Robert Atkins published Dr. Atkins Diet Revolution, which advocated the low-carbohydrate diet he had successfully used in treating patients in the 1960s (having developed the diet from a 1963 article published in JAMA).[citation needed] The book met with some success, but, because of research at that time suggesting risk factors associated with excess fat and protein, it was widely criticized by the mainstream medical community as being dangerous and misleading, thereby limiting its appeal at the time.[23] Among other things, critics pointed out that Atkins had done little real research into his theories and based them mostly on his clinical work. Later that decade, Walter Voegtlin and Herman Tarnower published books advocating the Paleolithic diet and Scarsdale diet, respectively, each meeting with moderate success.[24]

The concept of the glycemic index was developed in 1981 by David Jenkins to account for variances in speed of digestion of different types of carbohydrates. This concept classifies foods according to the rapidity of their effect on blood sugar levels – with fast-digesting simple carbohydrates causing a sharper increase and slower-digesting complex carbohydrates, such as whole grains, a slower one.[25] The concept has been extended to include the amount of carbohydrate actually absorbed, as well, as a tablespoonful of cooked carrots is less significant overall than a large baked potato (effectively pure starch, which is efficiently absorbed as glucose), despite differences in glycemic indices.
1990s – present
In the 1990s, Atkins published Dr. Atkins New Diet Revolution, and other doctors began to publish books based on the same principles. This has been said to be the beginning of what the mass media call the "low carb craze" in the United States.[26] During the late 1990s and early 2000s, low-carbohydrate diets became some of the most popular diets in the US. By some accounts, up to 18% of the population was using one type of low-carbohydrate diet or another at the peak of their popularity,[27] and this use spread to many countries. These were noted by some food manufacturers and restaurant chains as substantially affecting their businesses (notably Krispy Kreme).[28] Most of the mainstream medical community continued to denounce low-carbohydrate diets as being dangerous to health.[29][30][31] The low-carbohydrate advocates did some adjustments of their own, increasingly advocating controlling fat and eliminating trans fat.[32][33]

Many of the diet guides and their proponents who appeared at this time intentionally distanced themselves from Atkins and the term 'low carb' (because of the controversies), though their recommendations were based on largely the same principles (e.g., the Zone diet).[34][35] As a result, it is often a matter of debate which diets are really low-carbohydrate and which are not. The 1990s and 2000s also saw the publication of an increased number of clinical studies regarding the effectiveness and safety (pro and con) of low-carbohydrate diets (see low-carbohydrate diet medical research).

In the United States, the popularity of the low-carb diet trend waned somewhat in the late 2000s.[citation needed] Despite the decline in popularity, this diet trend has continued to quietly garner attention in the medical and nutritional science communities, and also inspired a number of hybrid diets that include traditional calorie-counting and exercise regimens.[7][36][37][38] Other popular low-carb diets focus on the removal of certain foods from the diet, such as sugar and grain.
Practices and theories

Today, the term "low-carbohydrate diet" is most strongly associated with the Atkins diet and other diets that share similar principles. The American Academy of Family Physicians defines low-carbohydrate diets as diets that restrict carbohydrate intake to 20 to 60 grams per day, typically less than 20% of caloric intake.[39]

[Jhanananda]

The low-carbohydrate diet continues to be the core of my recovery from diabetes; however, it has became clear to me that it was not a complete solution.  I needed chromium supplementation, which I got from eating three eggs a day, which are also 0-carb.

Seeing that the low-carbohydrate diet, which includes eggs, and nutritional yeast, has literally cured my diabetes; I now realize that an ovo-lacto vegetarian diet, which includes eggs and nutritional yeast, could be a reasonably healthy diet, as long as the grains and beans that are typical of the vegetarian diet are avoided; because even the whole grains and beans that vegetarians tend to eat, are still too high in carbohydrates.  This means low carb vegetables could supplement the low-carbohydrate diet without compromising that diet system, and thus lead to diabetes.

[Jhanananda]

From doing some Google searches or the nutritional value of various foods, I found that olives are a low carb food.  Also, anthocyanins can also be found in naturally ripened olives,[24][25] and are partly responsible for the red and purple colors of some olives.[24]

The olive (Listeni/ˈɒlɪv/ or Listeni/ˈɑːləv/, Olea europaea, meaning "olive from/of Europe") is a species of small tree in the family Oleaceae, found in much of Africa, the Mediterranean Basin from Portugal to the Levant, the Arabian Peninsula, and southern Asia as far east as China, as well as the Canary Islands, Mauritius and Réunion. The species is cultivated in many places and considered naturalized in France, Corsica, Greece, Crimea, Egypt, Iran, Iraq, Israel, Italy, Jordan, Palestine, Syria, Lebanon, Java, Norfolk Island, California and Bermuda.[1][2]

The olive's fruit, also called the olive, is of major agricultural importance in the Mediterranean region as the source of olive oil. The tree and its fruit give its name to the plant family, which also includes species such as lilacs, jasmine, Forsythia and the true ash trees (Fraxinus). The word derives from Latin ŏlīva ("olive fruit", "olive tree"; "olive oil" is ŏlĕum)[3] which is cognate with the Greek ἐλαία (elaía, "olive fruit", "olive tree") and ἔλαιον (élaion, "olive oil").[4][5] The oldest attested forms of the latter two words in Greek are respectively the Mycenaean 𐀁𐀨𐀷, e-ra-wa, and 𐀁𐀨𐀺, e-ra-wo or 𐀁𐁉𐀺, e-rai-wo, written in the Linear B syllabic script.[6][7] The word "oil" in multiple languages ultimately derives from the name of this tree and its fruit.

History
Prehistory

The edible olive has been cultivated for at least 5,000 to 6,000 years,[14] with the most ancient evidence of olive cultivation having been found in Syria, Palestine, and Crete.[15] The olive tree is native to the Mediterranean region and Western Asia, and spread to nearby countries from there.

The immediate ancestry of the cultivated olive is unknown. It is assumed[by whom?] that Olea europaea may have arisen from O. chrysophylla in northern tropical Africa and that it was introduced into the countries of the Mediterranean Basin via Egypt and then Crete or the Levant, Syria, Tunisia and Asia Minor.[citation needed] Fossil Olea pollen has been found in Macedonia, Greece, and other places around the Mediterranean, indicating that this genus is an original element of the Mediterranean flora. Fossilized leaves of Olea were found in the palaeosols of the volcanic Greek island of Santorini (Thera) and were dated about 37,000 BP. Imprints of larvae of olive whitefly Aleurolobus (Aleurodes) olivinus were found on the leaves. The same insect is commonly found today on olive leaves, showing that the plant-animal co-evolutionary relations have not changed since that time.[16]

As far back as 3000 BC, olives were grown commercially in Crete; they may have been the source of the wealth of the Minoan civilization.[17]

Nutritional value per 100 g (3.5 oz)
Energy 609 kJ (146 kcal)
Carbohydrates 3.84 g
Sugars 0.54 g
Dietary fiber 3.3 g
Fat 15.32 g
Saturated 2.029 g
Monounsaturated 11.314 g
Polyunsaturated 1.307 g
Protein 1.03 g

Vitamins
Vitamin A equiv. (3%) 20 μg
beta-carotene (2%) 231 μg
lutein zeaxanthin 510 μg
Thiamine (B1) (2%) 0.021 mg
Riboflavin (B2) (1%) 0.007 mg
Niacin (B3) (2%) 0.237 mg
Vitamin B6 (2%) 0.031 mg
Folate (B9) (1%) 3 μg
Choline (3%) 14.2 mg
Vitamin E (25%) 3.81 mg
Vitamin K (1%) 1.4 μg
Trace metals
Calcium (5%) 52 mg
Iron (4%) 0.49 mg
Magnesium (3%) 11 mg
Phosphorus (1%) 4 mg
Potassium (1%) 42 mg
Sodium (104%) 1556 mg

According to the USDA, a single serving of 10 medium sized green olives contains the following:

Water (g)       25.6
Energy (kcal)            49
Protein (g)     0.35
Fat, total (g)  5.21
Carbohydrate (g)    1.31
Sugars, total (g)        0.18
Fiber, total dietary (g)         1.1
Cholesterol (mg)      0
Saturated fatty acids, total (g)      0.69
Monounsaturated fatty acids, total (g)   3.847
Polyunsaturated fatty acids, total (g)      0.444
Calcium (mg)            18
Copper (mg) 0.041
Iron (mg)        0.17
Magnesium (mg)      4
Phosphorus (mg)      1
Potassium (mg)         14
Selenium (mcg)        0.3
Sodium (mg)  529
Zinc (mg)        0.01
Vitamin A, RAE (mcg)          7
Vitamin B-6 (mg)       0.011
Choline, total (mg)   4.8
Vitamin E, alpha tocopherol (mg)            1.3
Folate, total (mcg)   1
Vitamin K (mcg)        0.5
Niacin (mg)   0.081
Riboflavin (mg)         0.002
Thiamin (mg)  0.007
Carotene, beta (mcg)        79
Cryptoxanthin, beta (mcg)            3
Lutein + zeaxanthin (mcg)  173

Health benefits of olives

    Traditionally, olives have been viewed as very healthy food. The fruit provides calories; contain significant amounts of plant-derived anti-oxidants, minerals, phyto-sterols, and vitamins.

    Olives are a moderate source of calories; 100 g of fruits provide just 115 calories. Their calorie content basically comes from fats. Nonetheless, the fruit composes healthy fat in the form of mono-unsaturated fatty acids (MUFA) like oleic acid (18:1) and palmitoleic acid (16:1) that help lower LDL or "bad cholesterol" and increase HDL or "good cholesterol" in the blood. Research studies suggest that Mediterranean diet, which is rich in monounsaturated fatty acids help to prevent coronary artery disease and strokes by favoring healthy blood lipid profile.

    Olive fruit contains tyrosol phenolic compounds such as oleuropein and oleocanthal. These compounds are responsible for its bitter and pungent taste. Oleocanthal, oleurpein, and its derivative hydroxytyrosol are nature’s most powerful anti-oxidants. Together with vitamin E and carotenoids, they play a vital role fighting against cancer, inflammation, coronary artery disease, degenerative nerve diseases, diabetes…etc.

    Studies suggest that oleocanthal has ibuprofen (NSAID) like ant-inflammatory activities. Mediterranean diet that uses olive and its oil may be responsible in part for the lower incidences of coronary artery disease.

    Olive contains a good amount of vitamin E. 100 g cured, and canned fruits provide 1.65 mg (11% of RDA) of α-tocopherol. Vitamin E is a powerful lipid soluble antioxidant, required for maintaining the integrity of cell membrane of mucus membranes and skin by protecting it from harmful oxygen-free radicals.

    In addition, the fruits contain good amounts of minerals like calcium, copper, iron, manganese, and zinc. Further, they are small sources of B-complex vitamins such as niacin, choline, and pantothenic acid.

    Oil expressed from these fruits is recognized as one of the healthiest edible oils since it contains less saturated fat, and composes linoleic (omega-6) and linolenic acid (omega-3) essential fatty acids at the recommended 8:1 ratio.

[Jhanananda]

Those of you who have been following my health research and experiments will know that I recently learned about the dawn phenomenon of diabetes, and wile investigating that I discovered that my blood sugar will rise the more hungry that I get.  I have also discovered that if I eat a low carb meal or snack, then my blood sugar will actually drop. 

The low carb snacks that I eat are:

peanut butter on celery
cottage cheese with black olives.

Black olives have the additional benefit of containing significant levels of Anthocyanin, which is a natural anti-inflammatory, and research has shown that some type 2 diabetes are due to an underlying inflammation.

[Jhanananda]

Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity

Abstract

A novel hypothesis of obesity is suggested by consideration of diet-related inflammation and evolutionary medicine. The obese homeostatically guard their elevated weight. In rodent models of high-fat diet-induced obesity, leptin resistance is seen initially at vagal afferents, blunting the actions of satiety mediators, then centrally, with gastrointestinal bacterial-triggered SOCS3 signaling implicated. In humans, dietary fat and fructose elevate systemic lipopolysaccharide, while dietary glucose also strongly activates SOCS3 signaling. Crucially however, in humans, low-carbohydrate diets spontaneously decrease weight in a way that low-fat diets do not. Furthermore, nutrition transition patterns and the health of those still eating diverse ancestral diets with abundant food suggest that neither glycemic index, altered fat, nor carbohydrate intake can be intrinsic causes of obesity, and that human energy homeostasis functions well without Westernized foods containing flours, sugar, and refined fats. Due to being made up of cells, virtually all “ancestral foods” have markedly lower carbohydrate densities than flour- and sugar-containing foods, a property quite independent of glycemic index. Thus the “forgotten organ” of the gastrointestinal microbiota is a prime candidate to be influenced by evolutionarily unprecedented postprandial luminal carbohydrate concentrations. The present hypothesis suggests that in parallel with the bacterial effects of sugars on dental and periodontal health, acellular flours, sugars, and processed foods produce an inflammatory microbiota via the upper gastrointestinal tract, with fat able to effect a “double hit” by increasing systemic absorption of lipopolysaccharide. This model is consistent with a broad spectrum of reported dietary phenomena. A diet of grain-free whole foods with carbohydrate from cellular tubers, leaves, and fruits may produce a gastrointestinal microbiota consistent with our evolutionary condition, potentially explaining the exceptional macronutrient-independent metabolic health of non-Westernized populations, and the apparent efficacy of the modern “Paleolithic” diet on satiety and metabolism.

[Jhanananda]

Another name for the various low-carbohydrate diets is the Ketogenic Diet.  The origins of the Ketogenic Diet is in the treatment of epilepsy in children.

The ketogenic diet is a high-fat, adequate-protein, low-carbohydrate diet that in medicine is used primarily to treat difficult-to-control (refractory) epilepsy in children. The diet forces the body to burn fats rather than carbohydrates. Normally, the carbohydrates contained in food are converted into glucose, which is then transported around the body and is particularly important in fuelling brain-function. However, if there is very little carbohydrate in the diet, the liver converts fat into fatty acids and ketone bodies. The ketone bodies pass into the brain and replace glucose as an energy source. An elevated level of ketone bodies in the blood, a state known as ketosis, leads to a reduction in the frequency of epileptic seizures.[1]

The original therapeutic diet for paediatric epilepsy provides just enough protein for body growth and repair, and sufficient calories[Note 1] to maintain the correct weight for age and height. This classic ketogenic diet contains a 4:1 ratio by weight of fat to combined protein and carbohydrate. This is achieved by excluding high-carbohydrate foods such as starchy fruits and vegetables, bread, pasta, grains and sugar, while increasing the consumption of foods high in fat such as nuts, cream and butter.[1]

Most dietary fat is made of molecules called long-chain triglycerides (LCTs). However, medium-chain triglycerides (MCTs)—made from fatty acids with shorter carbon chains than LCTs—are more ketogenic. A variant of the classic diet known as the MCT ketogenic diet uses a form of coconut oil, which is rich in MCTs, to provide around half the calories. As less overall fat is needed in this variant of the diet, a greater proportion of carbohydrate and protein can be consumed, allowing a greater variety of food choices.[2][3]

Almost half of children and young people with epilepsy who have tried some form of this diet saw the number of seizures drop by at least half, and the effect persists even after discontinuing the diet.[4] The most common adverse effect is constipation, affecting about 30% of patients—this was due to fluid restriction, which was once a feature of the diet, but this led to increased risk of kidney stones, and is no longer considered beneficial.[4][5] There is some evidence that adults with epilepsy may benefit from the diet, and that a less strict regimen, such as a modified Atkins diet, is similarly effective.[1] Clinical trials and studies in animal models (including C. elegans[6]) suggest that ketogenic diets provide neuroprotective and disease-modifying benefits for a number of adult neurodegenerative disorders.[7][8] As of 2012, there is limited clinical trial data in these areas, and, outside of paediatric epilepsy, use of the ketogenic diet remains at the research stage.[5][9][10]

Diet

In 1921, Rollin Woodyatt reviewed the research on diet and diabetes. He reported that three water-soluble compounds, β-hydroxybutyrate, acetoacetate and acetone (known collectively as ketone bodies), were produced by the liver in otherwise healthy people when they were starved or if they consumed a very low-carbohydrate, high-fat diet. Russel Wilder, at the Mayo Clinic, built on this research and coined the term ketogenic diet to describe a diet that produced a high level of ketone bodies in the blood (ketonemia) through an excess of fat and lack of carbohydrate. Wilder hoped to obtain the benefits of fasting in a dietary therapy that could be maintained indefinitely. His trial on a few epilepsy patients in 1921 was the first use of the ketogenic diet as a treatment for epilepsy.[13]

Wilder's colleague, paediatrician Mynie Peterman, later formulated the classic diet, with a ratio of one gram of protein per kilogram of body weight in children, 10–15 g of carbohydrate per day, and the remainder of calories from fat. Peterman's work in the 1920s established the techniques for induction and maintenance of the diet. Peterman documented positive effects (improved alertness, behaviour and sleep) and adverse effects (nausea and vomiting due to excess ketosis). The diet proved to be very successful in children: Peterman reported in 1925 that 95% of 37 young patients had improved seizure control on the diet and 60% became seizure-free. By 1930, the diet had also been studied in 100 teenagers and adults. Clifford Barborka, also from the Mayo Clinic, reported that 56% of those older patients improved on the diet and 12% became seizure-free. Although the adult results are similar to modern studies of children, they did not compare as well to contemporary studies. Barborka concluded that adults were least likely to benefit from the diet, and the use of the ketogenic diet in adults was not studied again until 1999.[13][17]

MCT diet

In the 1960s, it was discovered that medium-chain triglycerides (MCTs) produce more ketone bodies per unit of energy than normal dietary fats (which are mostly long-chain triglycerides).[18] MCTs are more efficiently absorbed and are rapidly transported to the liver via the hepatic portal system rather than the lymphatic system.[19] The severe carbohydrate restrictions of the classic ketogenic diet made it difficult for parents to produce palatable meals that their children would tolerate. In 1971, Peter Huttenlocher devised a ketogenic diet where about 60% of the calories came from the MCT oil, and this allowed more protein and up to three times as much carbohydrate as the classic ketogenic diet. The oil was mixed with at least twice its volume of skimmed milk, chilled, and sipped during the meal or incorporated into food. He tested it on twelve children and adolescents with intractable seizures. Most children improved in both seizure control and alertness, results that were similar to the classic ketogenic diet. Gastrointestinal upset was a problem, which led one patient to abandon the diet, but meals were easier to prepare and better accepted by the children.[18] The MCT diet replaced the classic ketogenic diet in many hospitals, though some devised diets that were a combination of the two.[13]

By 2007, the ketogenic diet was available from around 75 centres in 45 countries, and less restrictive variants, such as the modified Atkins diet, were in use, particularly among older children and adults. The ketogenic diet was also under investigation for the treatment of a wide variety of disorders other than epilepsy.[1]

Efficacy

The ketogenic diet reduces seizure frequency by more than 50% in half of the patients who try it and by more than 90% in a third of patients.[5] Three-quarters of children who respond do so within two weeks, though experts recommend a trial of at least three months before assuming it has been ineffective.[9] Children with refractory epilepsy are more likely to benefit from the ketogenic diet than from trying another anticonvulsant drug.[1] There is some evidence that adolescents and adults may also benefit from the diet.[9]

Adverse effects

The ketogenic diet is not a benign, holistic or natural treatment for epilepsy; as with any serious medical therapy, there may be complications. These are generally less severe and less frequent than with anticonvulsant medication or surgery.[29] Common but easily treatable short-term side effects include constipation, low-grade acidosis and hypoglycaemia if there is an initial fast. Raised levels of lipids in the blood affect up to 60% of children[38] and cholesterol levels may increase by around 30%.[29] This can be treated by changes to the fat content of the diet, such as from saturated fats towards polyunsaturated fats, and, if persistent, by lowering the ketogenic ratio.[38] Supplements are necessary to counter the dietary deficiency of many micronutrients.[5]

Long-term use of the ketogenic diet in children increases the risk of slowed or stunted growth, bone fractures and kidney stones.[5] The diet reduces levels of insulin-like growth factor 1, which is important for childhood growth. Like many anticonvulsant drugs, the ketogenic diet has an adverse effect on bone health. Many factors may be involved such as acidosis and suppressed growth hormone.[38] About 1 in 20 children on the ketogenic diet will develop kidney stones (compared with one in several thousand for the general population). A class of anticonvulsants known as carbonic anhydrase inhibitors (topiramate, zonisamide) are known to increase the risk of kidney stones, but the combination of these anticonvulsants and the ketogenic diet does not appear to elevate the risk above that of the diet alone.[39] The stones are treatable and do not justify discontinuation of the diet.[39] Johns Hopkins Hospital now gives oral potassium citrate supplements to all ketogenic diet patients, resulting in a sevenfold decrease in the incidence of kidney stones.[40] However, this empiric usage has not been tested in a prospective controlled trial.[9] Kidney stone formation (nephrolithiasis) is associated with the diet for four reasons:[39]

    Excess calcium in the urine (hypercalciuria) occurs due to increased bone demineralisation with acidosis. Bones are mainly composed of calcium phosphate. The phosphate reacts with the acid, and the calcium is excreted by the kidneys.[39]
    Hypocitraturia: the urine has an abnormally low concentration of citrate, which normally helps to dissolve free calcium.[39]
    The urine has a low pH, which stops uric acid from dissolving, leading to crystals that act as a nidus for calcium stone formation.[39]
    Many institutions traditionally restricted the water intake of patients on the diet to 80% of normal daily needs;[39] this practice is no longer encouraged.[5]

In adults, common side effects include weight loss, constipation, raised cholesterol levels and, in women, menstrual irregularities including amenorrhoea.[41]

Implementation

Implementing the diet can present difficulties for caregivers and the patient due to the time commitment involved in measuring and planning meals. Since any unplanned eating can potentially break the nutritional balance required, some people find the discipline needed to maintain the diet challenging and unpleasant. Some people terminate the diet or switch to a less demanding diet, like the modified Atkins diet (MAD) or the low-glycemic index treatment (LGIT) diet, because they find the difficulties too great.[42]

For patients who benefit, half achieve a seizure reduction within five days (if the diet starts with an initial fast of one to two days), three-quarters achieve a reduction within two weeks, and 90% achieve a reduction within 23 days. If the diet does not begin with a fast, the time for half of the patients to achieve an improvement is longer (two weeks) but the long-term seizure reduction rates are unaffected.[44]

Classic Diet

The ketogenic diet is calculated by a dietitian for each child. Age, weight, activity levels, culture and food preferences all affect the meal plan. First, the energy requirements are set at 80–90% of the recommended daily amounts (RDA) for the child's age (the high-fat diet requires less energy to process than a typical high-carbohydrate diet). Highly active children or those with muscle spasticity require more calories than this; immobile children require less. The ketogenic ratio of the diet compares the weight of fat to the combined weight of carbohydrate and protein. This is typically 4:1, but children who are younger than 18 months, older than 12 years, or who are obese may be started on a 3:1 ratio. Fat is energy-rich, with 9 kcal/g (38 kJ/g) compared to 4 kcal/g (17 kJ/g) for carbohydrate or protein, so portions on the ketogenic diet are smaller than normal. The quantity of fat in the diet can be calculated from the overall energy requirements and the chosen ketogenic ratio. Next, the protein levels are set to allow for growth and body maintenance, and are around 1 g protein for each kg of body weight. Lastly, the amount of carbohydrate is set according to what allowance is left while maintaining the chosen ratio. Any carbohydrate in medications or supplements must be subtracted from this allowance. The total daily amount of fat, protein and carbohydrate is then evenly divided across the meals.[37]

A computer program such as KetoCalculator may be used to help generate recipes.[47] The meals often have four components: heavy whipping cream, a protein-rich food (typically meat), a fruit or vegetable and a fat such as butter, vegetable oil or mayonnaise. Only low-carbohydrate fruits and vegetables are allowed, which excludes bananas, potatoes, peas and corn. Suitable fruits are divided into two groups based on the amount of carbohydrate they contain, and vegetables are similarly divided into two groups. Foods within each of these four groups may be freely substituted to allow for variation without needing to recalculate portion sizes. For example, cooked broccoli, Brussels sprouts, cauliflower and green beans are all equivalent. Fresh, canned or frozen foods are equivalent, but raw and cooked vegetables differ, and processed foods are an additional complication. Parents are required to be precise when measuring food quantities on an electronic scale accurate to 1 g. The child must eat the whole meal and cannot have extra portions; any snacks must be incorporated into the meal plan. A small amount of MCT oil may be used to help with constipation or to increase ketosis.[37]

The classic ketogenic diet is not a balanced diet and only contains tiny portions of fresh fruit and vegetables, fortified cereals and calcium-rich foods. In particular, the B vitamins, calcium and vitamin D must be artificially supplemented. This is achieved by taking two sugar-free supplements designed for the patient's age: a multivitamin with minerals and calcium with vitamin D.[5] A typical day of food for a child on a 4:1 ratio, 1,500 kcal (6,300 kJ) ketogenic diet comprises:[29]

    Breakfast: egg with bacon
    28 g egg, 11 g bacon, 37 g of 36% heavy whipping cream, 23 g butter and 9 g apple.
    Snack: peanut butter ball
    6 g peanut butter and 9 g butter.
    Lunch: tuna salad
    28 g tuna fish, 30 g mayonnaise, 10 g celery, 36 g of 36% heavy whipping cream and 15 g lettuce.
    Snack: keto yogurt
    18 g of 36% heavy whipping cream, 17 g sour cream, 4 g strawberries and artificial sweetener.
    Dinner: cheeseburger (no bun)
    22 g minced (ground) beef, 10 g American cheese, 26 g butter, 38 g cream, 10 g lettuce and 11 g green beans.
    Snack: keto custard
    25 g of 36% heavy whipping cream, 9 g egg and pure vanilla flavouring.

Other applications

The ketogenic diet may be a successful treatment for several rare metabolic diseases. Case reports of two children indicate that it may be a possible treatment for astrocytomas, a type of brain tumour. Autism, depression, migraine headaches, polycystic ovary syndrome and diabetes mellitus type 2 have also been shown to improve in small case studies.[21] There is evidence from uncontrolled clinical trials and studies in animal models that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including amyotrophic lateral sclerosis, Alzheimer's disease and Parkinson's disease,[21][63] and may be protective in traumatic brain injury and stroke.[7][8] Because tumour cells are inefficient in processing ketone bodies for energy, the ketogenic diet has also been suggested as a treatment for cancer,[64][65] including glioma.[66]

A 2013 review said that there is enough suggestion of potential benefit from ketogenic diets in cancer therapy that establishing clinical trials is probably warranted.[67] At present the only evidence of benefit is anecdotal, but designing effective trials to measure the effect of adopting a ketogenic diet could prove challenging.[68]

In March 2009, Axona was approved as a medical food by the US Food and Drug Administration for the "dietary management of the metabolic processes and nutritional requirements associated with mild to moderate Alzheimer's disease". Glucose metabolism by the brain is impaired in Alzheimer's disease, and it is proposed that ketone bodies may provide an alternative energy source. Caprylidene is a powdered form of a medium-chain triglyceride, specifically caprylic triglyceride.[69]

[Jhanananda]

In a recent letter from Michael Hawkins, he told me that he and his wife, Karen, have taken up a FODMAP diet plan, which is a variant on the low-carb diet.

FODMAPs are short chain carbohydrates (oligosaccharides), disaccharides, monosaccharides and related alcohols that are poorly absorbed in the small intestine. These include short chain (oligo-) saccharide polymers of fructose (fructans) and galactose (galactans), disaccharides (lactose), monosaccharides (fructose), and sugar alcohols (polyols) such as sorbitol, mannitol, xylitol and maltitol.

The term FODMAP is an acronym, deriving from "Fermentable Oligo-, Di-, Mono-saccharides And Polyols."[1] These carbohydrates are commonly found in the modern western diet. Some evidence has been presented that the restriction of these FODMAPs from the diet may have a beneficial effect for sufferers of irritable bowel syndrome and other functional gastrointestinal disorders (FGID). The low FODMAP diet was developed at Monash University in Melbourne by Peter Gibson and Susan Shepherd.[2][3]

A low FODMAP diet has been shown in studies to be efficacious for many individuals with FGID.

Pathophysiology of FGID

The basis of many functional gastrointestinal disorders (FGIDs) is distension of the intestinal lumen. Such luminal distension may induce pain, a sensation of bloating, abdominal distension and motility disorders. Therapeutic approaches seek to reduce factors that lead to distension, particularly of the distal small and proximal large intestine. Food substances that can induce distension are those that are poorly absorbed in the proximal small intestine, osmotically active, and fermented by intestinal bacteria with hydrogen (as opposed to methane) production. The small molecule FODMAPs exhibit these characteristics.[3]
FODMAP absorption

Poor absorption of most FODMAP carbohydrates is common to everyone. Any FODMAPs that are not absorbed in the small intestine pass into the large intestine, where bacteria ferment them. The resultant production of gas potentially results in bloating and flatulence. Most individuals do not suffer significant symptoms but some may suffer the symptoms of IBS. Restriction of FODMAP intake in the latter group has been found to result in improvement of symptoms.[10]

Fructose malabsorption and lactose intolerance may produce IBS symptoms through the same mechanism but, unlike with other FODMAPs, poor absorption is found only in a minority of people. Many who benefit from a low FODMAP diet need not restrict fructose or lactose. It is possible to identify these two conditions with hydrogen and methane breath testing and thus eliminate the necessity for dietary compliance if possible.[3][10]
FODMAP sources in the diet

The significance of sources of FODMAPs varies through differences in dietary groups such as geography, ethnicity and other factors.[3] Commonly used FODMAPs comprise the following:[11]

    oligosaccharides, including fructans and galacto-oligosaccharides;
    disaccharides, including lactose;
    monosaccharides, including fructose;
    polyols, including sorbitol, xylitol, and mannitol.

Fructans, galactans and polyols (mandatory restriction)
Sources of fructans

Sources of fructans include wheat (though spelt contains comparatively low amounts),[12] rye, barley, onion, garlic, Jerusalem and globe artichoke, asparagus, beetroot, chicory, dandelion leaves, leek, radicchio, the white part of spring onion, broccoli, brussels sprouts, cabbage, fennel and prebiotics such as fructooligosaccharides (FOS), oligofructose and inulin.[3][10][13][14]
Sources of galactans

Pulses and beans are the main dietary sources (though green beans, tofu and tempeh contain comparatively low amounts).[14][15]
Sources of polyols

Polyols are found naturally in some fruit (particularly stone fruits), including apples, apricots, avocados, blackberries, cherries, lychees, nectarines, peaches, pears, plums, prunes, watermelon and some vegetables, including cauliflower, mushrooms and mange-tout peas. They are also used as bulk sweeteners and include isomalt, maltitol, mannitol, sorbitol and xylitol.[3][10][14]
Fructose and lactose (discretionary restriction)
Sources of fructose

See: Foods with high fructose content
Sources of lactose

See: Avoiding lactose-containing products
Low-FODMAP diet suggested foods

When considering a diet that involves avoiding a long list of foods, it is beneficial to look at foods that are acceptable on the diet. Below are low-FODMAP foods typically tolerated categorized by food group.[14]

Vegetables: bamboo shoots, bell peppers, bok choy, cucumbers, carrots, corn, eggplant (aubergine), lettuce, leafy greens, pumpkin, potatoes, squash (butternut, winter), yams, tomatoes, zucchini (courgette)

Fruits: bananas, berries (not blackberries or boysenberries), cantaloupe, grapes, grapefruit, honeydew, kiwifruit, kumquat, lemon, lime, mandarin, orange, passion fruit, pawpaw, pineapple, rhubarb, tangerine, tomatoes

Protein: beef, chicken, canned tuna, eggs, egg whites, fish, lamb, pork, shellfish, turkey, cold cuts (all prepared without added FODMAP containing foods), nuts (not cashews or pistachios), nut butters, seeds

Dairy and non-dairy alternatives: lactose-free dairy, small amounts of: cream cheese, half and half, hard cheeses (cheddar, Colby, Parmesan, Swiss), mozzarella, sherbet, (almond milk, rice milk, rice-milk ice-cream)

Grains: wheat-free grains/wheat-free flours (including gluten-free grains, which are free of wheat, barley and rye) and products made with these (e.g. bagels, breads, crackers, noodles, pancakes, pastas, pretzels, waffles); corn flakes, cream of rice, grits, oats, quinoa, rice, tapioca, corn tortillas.

Beverage options: water, coffee and tea, low FODMAP fruit/vegetable juices (limit to ½ cup at a time)
Effectiveness and nutritional adequacy

Evidence from randomized trials indicates that a low FODMAP diet can help to treat irritable bowel syndrome in adults and in children.[4][5][6][7] A comprehensive systematic review and meta-analysis supports the efficacy of this diet in the treatment of functional gastrointestinal symptoms of IBS[8] although the evidence is less good for constipation.[9]

There is only a little evidence of effectiveness in treating functional symptoms in inflammatory bowel disease from small studies which are susceptible to bias.[16][17][18]

In common with other defined diets, the low FODMAP diet can be impractical to follow[18] and risks imposing an undue financial burden and worsening malnutrition.[19]

[Jhanananda]

My diet is not strictly no-carb, but very low carb at 2-10 grams of carbs per meal.  I am not sure if it has resulted in [urlhttps://en.wikipedia.org/wiki/Ketosis]ketosis[/url] or not, nor do I know whether [urlhttps://en.wikipedia.org/wiki/Ketosis]ketosis[/url] is a dietary goal.  My dietary goal is simply to control my blood sugar through diet, and it seems reasonable to me that simply reducing carb intake will keep my blood sugar from getting too high.  Doing so has worked so far.

[urlhttps://en.wikipedia.org/wiki/Ketosis]Ketosis[/url]
Ketosis /kɨˈtoʊsɨs/ is a metabolic state where most of the body's energy supply comes from ketone bodies in the blood, in contrast to a state of glycolysis where blood glucose provides most of the energy. It is characterised by serum concentrations of ketone bodies over 0.5 millimolar, with low and stable levels of insulin and blood glucose.[1][2] It is almost always generalized with hyperketonemia, that is, an elevated level of ketone bodies in the blood throughout the body. Ketone bodies are formed by ketogenesis when liver glycogen stores are depleted (or from metabolising medium-chain triglycerides[3]). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate,[4] and the levels of ketone bodies are regulated mainly by insulin and glucagon.[5] Most cells in the body can use both glucose and ketone bodies for fuel, and during ketosis, free fatty acids and glucose synthesis (gluconeogenesis) fuel the remainder.

Longer-term ketosis may result from fasting or staying on a low-carbohydrate diet, and deliberately induced ketosis serves as a medical intervention for intractable epilepsy.[6] In glycolysis, higher levels of insulin promote storage of body fat and block release of fat from adipose tissues, while in ketosis, fat reserves are readily released and consumed.[5][7] For this reason, ketosis is sometimes referred to as the body's "fat burning" mode.[8]

Cause
Ketoacidosis
Main article: Ketoacidosis

Ketone bodies are acidic, but acid-base homeostasis in the blood is normally maintained through bicarbonate buffering, respiratory compensation to vary the amount of CO2 in the bloodstream, hydrogen ion absorption by tissue proteins and bone, and renal compensation through increased excretion of dihydrogen phosphate and ammonium ions.[9] Prolonged excess of ketone bodies can overwhelm normal compensatory mechanisms, leading to acidosis if blood pH falls below 7.35.

There are two major causes of ketoacidosis:

    Most commonly, ketoacidosis is diabetic ketoacidosis (DKA), resulting from increased fat metabolism due to a shortage of insulin. It is associated primarily with type I diabetes, and may result in a diabetic coma if left untreated.[10]

    Alcoholic ketoacidosis (AKA) presents infrequently, but can occur with acute alcohol intoxication, most often following a binge in alcoholics with acute or chronic liver or pancreatic disorders. Alcoholic ketoacidosis occurs more frequently following methanol or ethylene glycol intoxication than following intoxication with uncontaminated ethanol.[11]

A mild acidosis may result from prolonged fasting or when following a ketogenic diet or a very low calorie diet.[12][13]
Diet

If the diet is changed from one that is high in carbohydrates to one that does not provide sufficient carbohydrate to replenish glycogen stores, the body goes through a set of stages to enter ketosis. During the initial stages of this process, blood glucose levels are maintained through gluconeogenesis, and the adult brain does not burn ketones. However, the brain makes immediate use of ketones for lipid synthesis in the brain. After about 48 hours of this process, the brain starts burning ketones in order to more directly use the energy from the fat stores that are being depended upon, and to reserve the glucose only for its absolute needs, thus avoiding the depletion of the body's protein store in the muscles.[14]

Ketosis is deliberately induced by use of a ketogenic diet as a medical intervention in cases of intractable epilepsy.[12] Other uses of low-carbohydrate diets remain controversial.[15][16] Induced ketosis or low-carbohydrate diet terms have very wide interpretation. Therefore, Stephen S. Phinney and Jeff S. Volek coined the term "nutritional ketosis" to avoid the confusion.[17][clarification needed]

Carbohydrate deprivation to the point of ketosis has been argued both to have negative[18] and positive effects on health.[19][20]
Mechanism

When glycogen stores are not available in the cells, fat (triacylglycerol) is cleaved to provide 3 fatty acid chains and 1 glycerol molecule in a process known as lipolysis. Most of the body is able to use fatty acids as an alternative source of energy in a process called beta-oxidation. One of the products of beta-oxidation is acetyl-CoA, which can be further used in the citric acid cycle. During prolonged fasting or starvation, or as the intentional result of a ketogenic diet, acetyl-CoA in the liver is used to produce ketone bodies instead, leading to a state of ketosis.[citation needed]

During starvation or a long physical training session, the body starts using fatty acids instead of glucose. The brain cannot use long-chain fatty acids for energy because they are completely albumin-bound and cannot cross the blood–brain barrier. Not all medium-chain fatty acids are bound to albumin. The unbound medium-chain fatty acids are soluble in the blood and can cross the blood–brain barrier.[21] The ketone bodies produced in the liver can also cross the blood–brain barrier. In the brain, these ketone bodies are then incorporated into acetyl-CoA and used in the citric acid cycle.[citation needed]

The ketone body acetoacetate will slowly decarboxylate into acetone, a volatile compound that is both metabolized as an energy source and lost in the breath and urine.
Diagnosis

Whether ketosis is taking place can be checked by using special urine test strips such as Ketostix. The strips have a small pad on the end which is dipped in a fresh specimen of urine. Within a matter of seconds, the strip changes color indicating the level of acetoacetate ketone bodies detected, which reflects the degree of ketonuria, which, in turn, can be used to give a rough estimation of the level of hyperketonemia in the body (see table below). Alternatively, some products targeted to diabetics such as the Abbott Precision Xtra or the Nova Max can be used to take a blood sample and measure the β-hydroxybutyrate ketone levels directly. Normal serum reference ranges for ketone bodies are 0.5–3.0 mg/dL, equivalent to 0.05–0.29 mmol/L.[22]

Also, when the body is in ketosis, one's breath may smell of acetone. This is due to the breakdown of acetoacetic acid into acetone and carbon dioxide which is exhaled through the lungs. Acetone is the chemical responsible for the smell of nail polish remover and some paint thinners.

Severity

The concentration of ketone bodies may vary depending on diet, exercise, degree of metabolic adaptation and genetic factors. Ketosis can be induced when a ketogenic diet is followed for more than 3 days. This induced ketosis is sometimes called nutritional ketosis.[17] This table shows the concentrations typically seen under different conditions[1]

blood concentration (millimolar)    Condition
< 0.2    not in ketosis
0.2 - 0.5    slight/mild ketosis
0.5 - 3.0    induced/nutritional ketosis
2.5 - 3.5    post-exercise ketosis
3.0 - 6.0    starvation ketosis
15 - 25    ketoacidosis

Note that urine measurements may not reflect blood concentrations. Urine concentrations will be lower with greater hydration, and after adaptation to a ketogenic diet the amount lost in the urine may drop while the metabolism remains ketotic. Most urine strips only measure acetoacetate, while when ketosis is more severe the predominant ketone body is β-hydroxybutyrate.[27] Unlike glucose, ketones are excerted into urine at any blood level. Ketoacidosis is a metabolic derangement that cannot occur in a healthy individual who can produce insulin, and should not be confused with physiologic ketosis.

Controversy

Some clinicians[28] regard eliminating carbohydrates as unhealthy and dangerous.[29] However, it is not necessary to eliminate carbohydrates from the diet in order to achieve a state of ketosis. Other clinicians regard ketosis as a safe biochemical process that occurs during the fat-burning state.[17] Ketogenesis can occur solely from the byproduct of fat degradation: acetyl-CoA. Ketosis, which is accompanied by gluconeogenesis (the creation of glucose de novo from pyruvate), is the specific state with which some clinicians are concerned. However, it is unlikely for a normal functioning person to reach life-threatening levels of ketosis, defined as serum beta-hydroxybutyrate (B-OHB) levels above 15 millimolar (mM) compared to ketogenic diets among non diabetics which "rarely run serum B-OHB levels above 3 mM."[30] This is avoided with proper basal secretion of pancreatic insulin. People who are unable to secrete basal insulin, such as type 1 diabetics and long-term type II diabetics, are liable to enter an unsafe level of ketosis, eventually resulting in a coma that requires emergency medical treatment.[citation needed]

The anti-ketosis conclusions have been challenged by a number of doctors and advocates of low-carbohydrate diets, who dispute assertions that the body has a preference for glucose and that there are dangers associated with ketosis.[31][32] The Inuit are often cited as an example of a culture that has lived for hundreds of years on a low-carbohydrate diet. However, in multiple studies the traditional Inuit diet has not been shown to be a ketogenic diet.[33][34][35][36] Not only have multiple researchers been unable to detect any evidence of ketosis resulting from the traditional Inuit diet, but the ratios of fatty-acid to glucose were observed to be well below the generally accepted level of ketogenesis.[33][34][35][36] Furthermore, studies investigating the fat yields from fully dressed wild ungulates, and the dietary habits of the cultures who rely on them, suggest that they are too lean to support a ketogenic diet.[37][38] With limited access to fat and carbohydrates, cultures such as the Nunamiut Eskimos—who relied heavily on caribou for subsistence—annually traded for fat and seaweed with coastal-dwelling Taremiut.[37]

Some Inuit consume as much as 15-20% of their calories from carbohydrates, largely from the glycogen found in raw meats.[33][34][35][39] Furthermore, the blubber, organs, muscle and skin of the diving marine mammals that the Inuit eat have significant glycogen stores that are able to delay postmortem degradation, particularly in cold weather.[40][41][42][43][44][45]

Whether a no-carbohydrate diet would be safe for non-Inuit is also disputed: Nick Lane [46] speculates that the Inuit may have a genetic predisposition allowing them to eat a ketogenic diet and remain healthy. According to this view, such an evolutionary adaptation would have been caused by environmental stresses.[47] This speculation is unsupported, however, in light of the many arctic explorers, including John Rae, Fridtjof Nansen, and Frederick Schwatka, who adapted to Inuit diets with no adverse effects.[48]

Schwatka specifically commented that after a 2- to 3-week period of adaptation to the Inuit diet he could manage "prolonged sledge journeys," including the longest sledge journey on record, relying solely on the Inuit diet without difficulty.[49] Furthermore, in a comprehensive review of the anthropological and nutritional evidence collected on 229 hunter-gatherer societies it was found that, "Most (73%) of the worldwide hunter-gatherer societies derived >50% (≥56–65% of energy) of their subsistence from animal foods, whereas only 14% of these societies derived >50% (≥56–65% of energy) of their subsistence from gathered plant foods," suggesting that the ability to thrive on low carbohydrate diets is widespread and not limited to any particular genetic predisposition.[50] While it is believed that carbohydrate intake after exercise is the most effective way of replacing depleted glycogen stores,[51][52] studies have shown that, after a period of 2–4 weeks of adaptation, physical endurance (as opposed to physical intensity) is unaffected by ketosis, as long as the diet contains high amounts of fat.[47] Some clinicians refer to this period of keto-adaptation as the "Schwatka Imperative" after the explorer who first identified the transition period from glucose-adaptation to keto-adaptation.[53] http://www.fao.org/wairdocs/other/ai215e/ai215e06.htm

The diet of the Inuit is perhaps oversimplified in order to simulate evidence supporting the viability of long term carbohydrate deprivation. In addition to the seaweed and glycogen carbohydrates mentioned above, the Inuit are able to access many plant sources as well. The stomach contents of caribou contain a large quantity of partially digested lichens and plants which were considered a delicacy. Reindeer moss and other lichens were also harvested directly. The extended daylight of the arctic summer led to a profusion of plant life, and plant parts including berries, roots and stems, as well as mushrooms were harvested. These could be preserved for use in winter, often by dipping in seal fat. [54]

[Jhanananda]

I plan to get Urine test strips to see of my metabolism is ketonic or not, and if so, if it is at a safe level.

Urine test strips
A urine test strip or dipstick test is a basic diagnostic tool used to determine pathological changes in a patient’s urine in standard urinalysis.[1]

A standard urine test strip may comprise up to 10 different chemical pads or reagents which react (change color) when immersed in, and then removed from, a urine sample. The test can often be read in as little as 60 to 120 seconds after dipping, although certain tests require longer. Routine testing of the urine with multiparameter strips is the first step in the diagnosis of a wide range of diseases. The analysis includes testing for the presence of proteins, glucose, ketones, haemoglobin, bilirubin, urobilinogen, acetone, nitrite and leucocytes as well as testing of pH and specific gravity or to test for infection by different pathogens.[2]

The test strips consist of a ribbon made of plastic or paper of about 5 millimetre wide, plastic strips have pads impregnated with chemicals that react with the compounds present in urine producing a characteristic colour. For the paper strips the reactants are absorbed directly onto the paper. Paper strips are often specific to a single reaction (e.g. pH measurement), while the strips with pads allow several determinations simultaneously.[2]

There are strips which serve different purposes, such as qualitative strips that only determine if the sample is positive or negative, or there are semi-quantitative ones that in addition to providing a positive or negative reaction also provide an estimation of a quantitative result, in the latter the colour reactions are approximately proportional to the concentration of the substance being tested for in the sample.[2] The reading of the results is carried out by comparing the pad colours with a colour scale provided by the manufacturer, no additional equipment is needed.[3]

This type of analysis is very common in the control and monitoring of diabetic patients.[2] The time taken for the appearance of the test results on the strip can vary from a few minutes after the test to 30 minutes after immersion of the strip in the urine (depending on the brand of product being used).

Semi-quantitative values are usually reported as: trace, 1+, 2+, 3+ and 4+; although tests can also be estimated as milligrams per decilitre. Automated readers of test strips also provide results using units from the International System of Units.[2]
Test method

The test method consists of immersing the test strip completely in a well mixed sample of urine for a short period of time, then extracting it from the container and supporting the edge of the strip over the mouth of the container to remove excess urine. The strip is then left to stand for the time necessary for the reactions to occur (usually 1 to 2 minutes), and finally the colours that appear are compared against the chromatic scale provided by the manufacturer.

An improper technique can produce false results, for example, leukocytes and erythrocytes precipitate at the bottom of the container and may not be detected if the sample is not properly mixed, and in the same way, if an excess of urine remains on the strip after it has been removed from the test sample, may cause the reagents to leak from the pads onto adjacent pads resulting in mixing and distortion of the colours. To ensure that this does not occur it is recommended the edges of the strip are dried on

[Michael Hawkins]

Hello Jeffrey and friends,

I've been on the FODMap diet for about a month and will continue until the end of the year.  Karen has been on it since Spring.  Mostly we avoid grains and starches that easily turn into sugar -- so no bread, no potatoes, no dairy, etc.  We are also restricted from eating certain veggies and fruits but are allowed all manner of meat.  We are on the diet for a couple reasons -- 1) to kill off yeast, and 2) to test for allergy-producing foods.  To assist in killing yeast, we are on high doses of garlic and probiotics.  At the end of the year I will slowly re-introduce various foods to see if I have a reaction, then endeavour to eliminate those foods from my diet moving forward.

I am losing weight, have good energy and am enjoying heightened clear-headedness as well as spontaneous insights around the issues and behaviors that produce suffering.  So, it is worth the time and energy required to re-program my eating habits.

[Jhanananda]

Hello, Michael, it is good to read a message from you.  Thank-you for sharing your experiments with the FODMap diet.

Yesterday I was greatly disappointed to find that my blood sugar was 178 for a low and 274 for a high.  This is after rigorously following a very low carb diet for 1.5 years.  Today I fasted, with the exception of a few small pieces of cheese that a friend felt the need to give me, even though I said I was fasting, but I did not feel I should reject his offer, and cheese, after all, is low carb (Total Carbohydrate 0.4 g).  However, my low and high today was only slightly better than yesterday's at 170-240.  I plan to just fast until my blood sugar returns to normal, then return to eating, but even a lower carb diet, while closely monitoring my blood sugar.  This dos not look good though.

[Jhanananda]

I used to eat about 50gms of carbs per day, which were mostly distributed in roughly 10-15 gram portions at each meal, with another 10-20 grams acquired through beverages throughout the day.  This diet resulted in normal blood sugar levels throughout last winter.

After I was done moving by May first I found my blood sugar had risen back into the 200+ range.  I attributed the rise in blood sugar to a disruption in my daily diet regimen, so I returned to my previous diet plan.  With the disruption in my lifestyle I did not test my blood sugar daily until 2 days ago when I found my blood sugar 200+.

I have since  eaten next to nothing, while my daily blood sugar is slowly lowering, it is still rising over 200.  So, I find I need to answer the question as to where the sugar is coming from. 

Role of Carbohydrates

The roles of carbohydrate in the body includes providing energy for working muscles, providing fuel for the central nervous system, enabling fat metabolism, and preventing protein from being used as energy. Carbohydrate is the preferred source of energy or fuel for muscle contraction and biologic work.

Foods containing carbohydrate are in the grains, fruit, and milk groups. Vegetables have a small amount of carbohydrate.

After carbohydrate is eaten, it is broken down into smaller units of sugar (including glucose, fructose and galactose) in the stomach and small intestine. These small units of sugar are absorbed in the small intestine and then enter the bloodstream where they travel to the liver. Fructose and galactose are converted to glucose by the liver. Glucose is the carbohydrate transported by the bloodstream to the various tissues and organs, including the muscles and the brain, where it will be used as energy.

If the body does not need glucose for energy, it stores glucose in the liver and the skeletal muscles in a form called glycogen. If glycogen stores are full, glucose is stored as fat. Glycogen stores are used as an energy source when the body needs more glucose than is readily available in the bloodstream (for example, during exercise). The body has limited storage capacity for glycogen (about 2000 calories), which is why carbohydrate is commonly referred to as the limiting fuel in physical performance.

Carbohydrate spares the use of protein as an energy source. When carbohydrate consumption is inadequate, protein is broken down to make glucose to maintain a constant blood glucose level. However, when proteins are broken down they lose their primary role as building blocks for muscles. In addition, protein breakdown may result in an increased stress on the kidneys, where protein byproducts are excreted into the urine.

Finally, glucose is essential for the central nervous system. The brain primarily uses glucose as its energy source, and a lack of glucose can result in weakness, dizziness, and low blood glucose (hypoglycemia). Reduced blood glucose during exercise decreases performance and could lead to mental as well as physical fatigue.

Three Places Where Carbs Are Stored in Body
Carbohydrates are your body’s most efficient fuel source...

Liver Glycogen
Glycogen stored in your liver primarily serves to maintain your blood sugar levels during an overnight fast. Changes in blood sugar levels activate or deactivate certain hormones such as insulin, glucagon and epinephrine to signal enzymes to stimulate glycogen synthesis or breakdown, depending on your fuel status...

Muscle Glycogen

The majority of the total amount of glycogen in your body exists in your muscle. Unlike liver glycogen, muscle glycogen breakdown does not increase specifically due to whether you are fasted. Instead, muscle glycogen breakdown increases in response to your muscles’ demand for ATP, or adenosine triphosphate, for cellular energy. The demand is particularly high during high-intensity exercise such as sprinting or weightlifting, which can only use carbs for fuel. However, elevated insulin levels from a high-carb meal will increase glucose uptake into muscle, which will increase ATP synthesis, reduce muscle cell energy demand and enable glycogen synthesis enzymes to form glycogen...

Carbs Stored In Fat Tissue

Additionally, certain intermediate molecules in carb metabolism can be converted to fat and stored in fat tissue. After you absorb single-sugar carbs into the bloodstream, your tissues must further break down the sugar into ATP, a form of energy your cells can use. This process involves multiple enzymatic reactions in the mitochondria. Depending on how much energy you need, some of the intermediate molecules of this process might be transported out and converted to triglycerides in your fat tissue. If your energy demands are low and sugar supply is high — for example, if you are watching TV and eating several candy bars — the extra sugars might begin to go through the breakdown process, but will eventually be transported out and stored as fat tissue...

So, apparently my body is extracting glycogen out of the liver, and muscles, and converting it to glucose, so that my blood sugar will not drop significantly until those glycogen stores are depleted.  At that point my metabolism is expected to enter ketosis.

[Jhanananda]

Sam posted this interesting link on his FaceBook page, Simple carbs linked to increased incidence of lung cancer

Researchers at The University of Texas MD Anderson Cancer Center found a 49 percent increased risk of lung cancer among those who consumed the greatest amount of high-glycemic foods

. 
References:

Dietary glycemic index linked to lung cancer risk in select populations

Consuming a diet with a high glycemic index, a classification of how rapidly carbohydrates elevate blood sugar levels, was independently associated with an increased risk of developing lung cancer in non-Hispanic whites, according to a new epidemiologic study from The University of Texas MD Anderson Cancer Center.

This research, published this week in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research, represents the largest study to investigate potential links between glycemic index (GI) and lung cancer. The findings also unveil for the first time that GI was more significantly associated with lung cancer risk in particular subgroups, such as never-smokers and those diagnosed with the squamous cell carcinoma (SCC) subtype of lung cancer.

Here I would want to also look at background levels of radiation, since my diabetes is more associated with background levels of radiation, than my consumption of carbohydrates; and the medical position on radon and other naturally occurring radiation has been directly associated with all non-smoker cases of lung cancer.

Can Certain 'Poor Carb' Diets Raise Nonsmokers' Lung Cancer Risk?

Dietary glycemic index linked to lung cancer risk in select populations

The above article had a link to another related article,
Moderate blood sugar levels increase the risk of cancer.

Diabetes must not be ignored. In fact, a surprise to most women, those with the highest glucose levels are 63% more likely to develop breast cancer. A study of 33,293 women – which measured fasting and after meal glucose spikes – found those in the highest range were 75% more likely to develop cancer.

References:

High Blood Sugar Linked to Cancer Risk

Swedish Study Shows More Cancer in People With Higher Blood Sugar, Regardless of Diabetes

Feb. 27, 2007 -- Women with high blood sugar may be more likely to develop cancer, even if they don't have diabetes, a Swedish study shows.

High blood sugar (hyperglycemia) wasn't tied to men's overall cancer risk.

But when researchers looked at specific types of cancer, they found that both men and women with the highest blood sugar levels were more likely to have pancreatic cancer, urinary tract cancer, and malignant melanoma (the most deadly type of skin cancer) than those with the lowest blood sugar levels.

Keeping blood sugar levels within the normal range "may reduce cancer risk," write the researchers, who included Par Stattin, MD, PhD, of Sweden's Umea University Hospital.

High Insulin and Sugar Increases Breast Cancer Risk

When it comes to breast cancer, insulin is no friend. One of the biggest reasons is due to the fact that both normal breast cells and cancer cells have insulin receptors on them. When insulin attaches to its receptor, it has the same effect as when estrogen attaches to its receptor; it causes cells to start dividing. The higher your insulin levels are, the faster your breast cells will divide; the faster they divide, the higher your risk of breast cancer is and the faster any existing cancer cells will grow.

Cancer & Sugar - Strategy for Selective Starvation of Cancer

According to researchers at the University of California, San Francisco, sugar poses a health risk—contributing to around 35 million deaths globally each year. So high is sugar's toxicity that it should now be considered a potentially toxic substance like alcohol and tobacco...

Sugar's harmful effects do not stop at diabetes, metabolic syndrome, hyper- and hypoglycemia, GERD and heart disease. Sugar and cancer are locked in a death grip, yet oncologists often fail to do what's necessary to stop their patients from feeding their cancers with sweets...

An increasing number of medical scientists and many alternative practitioners know that the most logical, effective, safe, necessary and inexpensive way to treat cancer is to cut off the supply of food to tumors and cancer cells, starving them with a lack of glucose. The therapeutic strategy for selective starvation of tumors by dietary modification (ketogenic diet) is one of the principle forms of therapy that is necessary for cancer patients to win their war on cancer.

Researchers at Huntsman Cancer Institute in Utah were one of the first to discover that sugar "feeds" tumors. The research published in the journal Proceedings of the National Academy of Sciences said, "It's been known since 1923 that tumor cells use a lot more glucose than normal cells. Our research helps show how this process takes place, and how it might be stopped to control tumor growth," says Don Ayer, Ph.D., a professor in the Department of Oncological Sciences at the University of Utah.

Dr. Thomas Graeber, a professor of molecular and medical pharmacology, has investigated how the metabolism of glucose affects the biochemical signals present in cancer cells. In research published June 26, 2012 in the journal Molecular Systems Biology, Graeber and his colleagues demonstrate that glucose starvation—that is, depriving cancer cells of glucose—activates a metabolic and signaling amplification loop that leads to cancer cell death as a result of the toxic accumulation of reactive oxygen species (ROS).[1]