Paleo Diet: Raw Paleo Diet and Lifestyle Forum
Raw Paleo Diet to Suit You => Omnivorous Raw Paleo Diet => Topic started by: ForTheHunt on April 24, 2010, 12:11:43 am
-
I just ate an apple and instantly I'm very tired
And it happens almost every time I eat fruit..
So I'm wondering if it's some sort of diabetes or what ever?
-
Same thing happens to me. The sweeter the fruit, the more tired I get. I think it's hypoglycemia (always had problems with that.)
-
Do you get the same reaction even if you eat it with fat?
-
Well, if you get this reaction with fruit, perhaps you should try raw zero carb after all.
-
I just ate an apple and instantly I'm very tired
And it happens almost every time I eat fruit..
So I'm wondering if it's some sort of diabetes or what ever?
Maybe your apple is poisoned.
You know, full of chemicals.
If your apple is pure, then the apple is not for you.
-
I don't generally notice it that quickly from a single apple, but if I overdo it on carbs then I often have trouble digesting and do tend to get tired within an hour afterward. Within several hours or the next morning I tend to start yawning. I remember a dentist asked me years ago if I experienced any fatigue or other symptoms for his checkoff review and I reported getting tired after lunch, but he said that was "normal." Well, it doesn't happen anymore as long as I avoid carbs (whether cooked or raw), so I guess I'm "abnormal" now. ;D
I tried eating raw animal or plant fat with carbs like raw fruits or raw honey and it didn't eliminate my symptoms (although sometimes fat prevents or stops the yawning if I eat enough of it during or afterward--but I still tend to get acne, dry skin, white dental crud, morning breath, etc.). The worst of my symptoms from carbs usually become apparent the next morning after eating them. Does eating fat with carbs work 100% for anyone here who normally has a problem with carbs?
Dr. Harris has suggested that people who are hypersensitive to carbs like Lex and me might have insulin resistance (which can lead to type II diabetes), though no physician has diagnosed me with that (but they never checked specifically for it either).
-
What kinds of fruit? Have you tried lower sugar fruits?
-
Does eating fat with carbs work 100% for anyone here who normally has a problem with carbs?
It's helped alleviate some of the problems but only by maybe 20%.
I still get all of the other problems though.
-
What kinds of fruit? Have you tried lower sugar fruits?
All kinds tested so far including lower sugar fruits like berries. I'm hoping that maybe I'll have better luck with wild berries this summer. Fingers crossed.
-
Do not accept an apple from your wicked stepmother.
Unless you wish to sleep for a very long time...
-
What about veggies?
-
I just ate an apple and instantly I'm very tired
And it happens almost every time I eat fruit..
So I'm wondering if it's some sort of diabetes or what ever?
It is hypoglycaemia. I had the same trouble when I was on a carnivorous diet. On a zero carb diet, my body seems to lost the ability to process carbs correctly (loss of enzymes, bacteria, hormones, insulin resistance?). After slowly reintroducing fruits, I can now eat them without problem as long as I eat just a few at once (i.e : one banana).
-
I agree, you have to keep eating some fruit because the body will discontinue the production of enzymes that are not needed. The same happens to the salivary enzymes, most of them are spared on a raw diet.
-
I had the same trouble when I was on a carnivorous diet. On a zero carb diet, my body seems to lost the ability to process carbs correctly (loss of enzymes, bacteria, hormones, insulin resistance?).
I see that as one of the gifts of zero carb. Our bodies recognize and reject sugars.
-
I see that as one of the gifts of zero carb. Our bodies recognize and reject sugars.
That's not it. Too many people who have no issues have gone VLC or raw zero-carb for lengthy periods and then gradually lost the ability to digest raw carbs solely because the body stopped providing the right enzymes or bacteria to properly digest them. The same sort of thing happens often to long-term raw vegans who, after years of never eating any animal foods, start experiencing great difficulty in digesting animals foods when they reintroduce them into their diets - until, after a while, they get used to them as their body redadapts to their digestion once again.
-
What fruits ? What's the ratio of glycose to fructose in these fruits ? Maybe you are fructose intolerance - unable to handle fructose.
-
I see that as one of the gifts of zero carb. Our bodies recognize and reject sugars.
Why would he reject sugar, one of the 2 main fuel ?
-
Fat is the best fuel, sugar is inferior. I have had my best energy doing fasted hiking, or lifting weights, being zero carb, than when I was high carb or VLC and using protein shakes.
-
I agree, fat is the best fuel for the body. But my mind seems to do poorly if I don't get sufficient carbs
-
I agree, fat is the best fuel for the body. But my mind seems to do poorly if I don't get sufficient carbs
I noticed this after prolonged work with my brain where I had to think 5 hours straight. It made me so dizzy and tired at evening. So I was thinking if the symptoms were because of decreased glycogen stores.
Brain uses more ketones over time if body is constantly in keto state. If I am right then after 40 days brain will use 60% of it's energy from ketones so as my brain was still used with glycose it might have used all my glycogen stores and made me dizzy until they were filled again. Just a theory.
-
Fat is the best fuel, sugar is inferior. I have had my best energy doing fasted hiking, or lifting weights, being zero carb, than when I was high carb or VLC and using protein shakes.
You are generalizing your personal experience.
The truth is there is no better fuel : there are 2 complementary fuels, fat and sugar, that we are evolved to use as source of calories.
-
Nobody here yet used the expressions "insulin sensitivity" and "leptin sensitivity".
Low-carb diets apparently blunt insulin sensitivity and don't do anything for leptin sensitivity, plus the so-called glycation associated with hi-carb diets is only understood to occur where there are high tissue cell membrane PUFA concentrations, which are highly unstable (hence the PUFAs are the mediator in tissue protein glycation/crosslinking, high hba1c etc.).
Overfeeding studies (more-than-energy-maintenance calories per day) have demonstrated that a high carbohydrate diet can improve both insulin and leptin sensitivity. The Kitavans are the fine example with their low-PUFA, hi-carb and generally still nutrient dense diet, which is worth consideration and has not yet really been debunked yet.
I love how the wisdom of the primitive isolates just flies in the ivory-tower-face of all these hypothetical, half-baked models and assumptions...
The question would be then: how much fruit year-round did paleo man eat from his local landbase, given the seasonal nature and lack of preservative technology? Also, how much sugar did the original, wild, heirloom, seeded fruits contain? Is it possible that our domesticated fruits are a plague to us, even though they still retain their nice colours/profile?
Damned if we do, damned if we don't...
-
Oh, also, there's the context of the metabolism as representative of the hormone signalling systems stimulated by the dynamic correlation with how much food is around at a given time (considering that the heavily refined human organism is an extremely robust survival mechanism)...Hence the overfeeding (3000-4000 calories) studies demonstrating that insulin and leptin sensitivity improve, along with basal metabolic rate and body compostion. Imagine very stable thermogenesis from excess calories as opposed to adiposity to the extent of obesity.
The other point is, why do most hunter-gatherer tribes utilise everything on their landbase, including hi-carb starches? Is it possibly because everything contributes to survival of the population and the birth of new generations (e.g. females gaining adiposity when trying to conceive) - that is, they're in dynamic equilibrium with their ecosystem (even though we're opportunist omnivores).
-
Here's one report, that I found in a few seconds of Googling...
Scientists at Beth Israel Deaconess Medical Center (BIDMC) have shown that restoring leptin sensitivity to a tiny area of POMC neurons in the brain’s hypothalamus cures mice deficient in the leptin-receptor of severe diabetes, and also spontaneously doubles their activity levels.
Writing about their findings in the journal Cell Metabolism, the researchers say that their findings may help further expand the understanding as the leptin’s role in the brian’s complex neurocircuitry behind weight gain and glucose control.
“This discovery suggests a new therapeutic pathway for drugs to treat insulin-resistant diabetes in humans with severe obesity, and possibly even to stimulate their urge to exercise,” says Dr. Christian Bjorbaek, a researcher in the Division of Endocrinology, Diabetes and Metabolism at BIDMC and Associate Professor of Medicine at Harvard Medical School.
“We know that the majority of humans with Type 2 diabetes are obese and that weight loss can often ameliorate the disease. However, in many cases, it’s difficult for these individuals to lose weight and can keep weight off. If, as these findings suggest, there is a system in the brain that can control blood-glucose directly, it offers hope for the identification of novel anti-diabetic drug targets,” Bjorbaek added.
Leptin, which was first identified in 1994 as an appetite and weight-regulation hormone, is known to play a key role in energy homeostasis through its effects on the central nervous system.
Previously conducted studies have already shown that a region of the brain’s hypothalamus, known as the arcuate nucleus (ARC), is one key area where leptin exerts its influence.
Within the ARC, scientists have also identified two types of leptin-responsive neurons: the Agouti-related peptide (AgRP) neurons, which stimulate appetite and the pro-opiomelanocortin (POMC) neurons, which curb appetite.
“Still other studies had indicated that, by way of the ARC, leptin also had a function in both blood-sugar control and in activity levels. We hypothesized that, in both cases, the POMC neurons were involved,” says Bjorbaek.
He reveals that with a view to testing their hypothesis, the research team studied a group of leptin-receptor-deficient laboratory mice.
“The animals were severely obese and profoundly diabetic. Using Cre-Lox technology we were able to genetically and selectively re-express leptin receptors only in the POMC neurons. When leptin receptor activity was restored to just this very small group of neurons, the mice began eating about 30 percent fewer calories and lost a modest amount of weight,” he says.
Bjorbaek further reveals that the animals’ blood sugar levels returned to normal independent of any change in weight or eating habits, and their activity levels spontaneously doubled.
-
So laughably, lo-carb seems like a sticking plaster (y'know, treating the symptoms rather than underlying cause), possibly while the problem of blunted insulin sensitivity and leptin sensitivity remains.
Insulinteresting, to say the least...;-))
By the way, this does not mean that I eat a large proportion of my calories as carbs - I'm just trying to understand what could be an optimal proportion, particularly for keeping the metabolism stoked with optimal insulin/leptin sensitivity (the raw thyroid experiment definitely won't be repeated any time soon).
Personally, I think it takes a while to improve glucose tolerance after lo-carbing, but mine seems to have improved over a few weeks.
That said, I still yawn after meals (like hypoglycaemic yawnorama), so I'm thinking about obtaining a BG meter to do post-prandial and fasting levels.
-
Here's another one about rodent endocrinology...
For the first time, terminally ill rodents with type-1 diabetes have been restored to complete health with a single injection of a substance other than insulin.
University of Texas Southwestern (UTS) researchers tested for the first time whether an injection of leptin gene given to insulin-deficient mice dying of diabetic coma could reverse their terminal condition.
After the injection, the animals began producing excessive amounts of leptin, which reversed consequences of type-1 diabetes including weight loss, hyperglycemia and ketoacidosis, a potentially fatal condition that develops when the body doesn’t have enough insulin to meet basic metabolic requirements.
Much of the effect was mediated by complete suppression of the high glucagon levels, said Xinxin Yu, assistant instructor of UTS internal medicine and co-author of the study.
“These animals were actually dying,” Yu said. “But if we gave them the leptin gene, within two weeks, the terminally ill rodents were restored to full health without any other treatment.”
Since the discovery of insulin in 1922, type-1 diabetes (insulin-dependent diabetes) in humans has been treated by injecting insulin to lower high blood sugar levels and prevent diabetic coma.
“The fact that these animals don’t die and are restored to normal health despite a total lack of insulin is hard for many researchers and clinicians to believe,” said Roger Unger, professor of internal medicine and senior study co-author.
“Many scientists, including us, thought it would be a waste of time to give leptin in the absence of insulin. We’ve been brainwashed into thinking that insulin is the only substance that can correct the consequences of insulin deficiency.”
The mechanism of leptin’s glucose-lowering action appears to involve the suppression of glucagon, a hormone produced by the pancreas that raises glucose levels.
The next step is to study other potential glucagon suppressants and begin leptin clinical trials within the next year, said an UTS release.
These findings appear in the Proceedings of the National Academy of Sciences.
-
Another thing I read somewhere recently is that fructose is tenfold more glycating in the presence of PUFA than glucose, although with typical human anatomy, fructose should not enter the general circulation directly because its metabolic pathway includes first the hepatic portal system, then the liver (lipogenesis etc.). However, one may understand that an over-permeable intestine (leaky gut syndrome) may allow passage of fructose into the general circulation, like all of these other weird opioid peptides that can even cross the blood/brain barrier (e.g. casein, gliadin, glutenin etc.). If the fructose can enter the general circulation and contribute to glycation of high-PUFA cell membranes, the result would be inflammation. It's established that inflammation is a factor in insulin resistance disease, so maybe the fructose is a deleterious factor in the equation (as could be glucose, to a lesser extent). It really underscored the point about eliminating all PUFA except the trace amounts in ruminant meat/fat/organs.
One wonders if a starchy or low-fructose fruit (banana, berries etc.) would be more optimal for those recovering from this chaotic interaction of factors in the vicious circle.
Also, to improve insulin and leptin sensitivity, maybe one could eat 30 bananas per day (no reference to the 80/10/10 site!!!), with an arbitrary amount at each sitting (of course, not that I'm suggesting that).
Another thing that crossed my mind is why don't all these scientists/endocrinologists appear on this forum, agreeing with us on AGE accumulation in the cellular substrates (causing inflammation etc.)? (joining the cult, so to speak) Is it really just the wisdom/experience of anecdote that prevails yet again like the bygone generations of HGs? Rather quaint methinks...
-
How do you get "high tissue cell membrane PUFA concentrations"?
-
Err...consuming anything with > 3% PUFA (e.g. olive oil = 10% PUFA)...That would include poultry and pork fattened on grains! Ruminants don't accumulate PUFAs, so grain-fed ruminants don't present this problem, although you'd be missing out on things like CLA from grass-fed ruminants, not to mention minerals and other things...
-
So, if one only consumes grainfed meat+fat, than eating lots of fruits is bad? what if it's mixed?
Where did you get the "3%" PUFA limit?
-
What about veggies?
Yeah, I can eat some veg, but I'm not big on the taste of most veg other than mustard and beet greens, radish, young chervil, young arugula, green cabbage, broccoli, garlic, and ginger, so my amounts of veg tend to be small (I eat mostly mesclun young greens mix, herb/greens mix, cabbage and young spinach because they taste OK or good to me raw, provide some taste variety and probably provide a little nutrition and alkaline pH even when raw, help friends, relatives and strangers to avoid bugging me about my "strange" diet, and are available in my local market) and from an Instincto perspective I shouldn't force myself to eat a lot of food I don't like the taste of anyway (and I tend to dislike cooked veggies even more, except for yellow onions, which taste sweeter to me and cause less heartburn when cooked). Dislike of veg seems to run in my family, as my father dislikes them even more than I do and his mother was not big on veg.
What fruits ? What's the ratio of glycose to fructose in these fruits? Maybe you are fructose intolerance - unable to handle fructose.
That's a possibility, and it's interesting that Gary Taubes and others have suggested that fructose might be more of a problem for humans than other sugars, based on some studies and metabolic analyses (relax Tyler, I don't know whether or not this is true, so I'm not arguing it myself). Some sites identify these fruits as relatively low in fructose: kumquat, grapefruit, lemons, limes, pineapples, strawberries, raspberries, blackberries, lemons, limes, avocado, bananas, rhubarb, orange. Unfortunately I haven't done well when I tried citrus fruits (canker sores, stomach upset, worsened dental problems, etc.) or even berries (I seem to be able to handle about a small handful once a week or so, so I don't buy whole pints any more--just occasionally grab a few from the cafeteria as a treat with some young greens and olive oil to try to offset any negative effects). I seem to be able to handle one small banana now and then, but if I eat too many I paradoxically get potassium deficiency as well as acne, dental crud and other symptoms. I've also noticed that if I eat fruit with my raw meat and fat that the fruit cancels out the euphoria from the meat/fat, which is a bummer.
In my case the sensitivity to fruit was there before I went ZC and each reduction of raw whole fruit in my diet provided additional benefits. I wish it weren't so. Luckily I haven't noticed any increase in problems from fruits after 14 months of VLC to ZC like some others have, but perhaps that still could happen in the future and Dr. Harris does suggest that VLCers have reduced ability to handle blood sugar spikes from excessive carb consumption at one sitting. I hope to eat a little fruit now and then, mostly in season, to try to prevent worsened intolerance. I think I may have a carb or fructose intolerance or both. Raw fruit is apparently not healthy for people with carb or fructose intolerance and thus shouldn't be promoted as purely healthy and free of side effects for everyone.
...The Kitavans are the fine example with their low-PUFA, hi-carb and generally still nutrient dense diet, which is worth consideration and has not yet really been debunked yet.
I love how the wisdom of the primitive isolates just flies in the ivory-tower-face of all these hypothetical, half-baked models and assumptions...
Hooray for the Kitavans. My real world experience is that I eat a diet high in saturated and monounsaturated fats (my main fat is suet), yet carbs still bother me--even if I eat them with suet or marrow, though a little less so. I even tried a sort of muktuk (berries and water mixed into warm tallow). I'm not looking for an argument. If you do well on carbs then by all means eat them--leaves more meat and fat for me. :D
The question would be then: how much fruit year-round did paleo man eat from his local landbase, given the seasonal nature and lack of preservative technology? Also, how much sugar did the original, wild, heirloom, seeded fruits contain? Is it possible that our domesticated fruits are a plague to us, even though they still retain their nice colours/profile? ...
Plus there are regional and individual differences in genetics and epigenetics that apparently affect how much carbs one can tolerate. I doubt the Inuit or Chukchi would do as well as the Kitavans on the Kitavan diet, or vice-versa.
The other point is, why do most hunter-gatherer tribes utilise everything on their landbase, including hi-carb starches?
As I've discussed before, just because HGs or wild animals eat a food doesn't guarantee that it's optimally healthy for them. It's a clue that it might be healthy, but not a guarantee. So the fact that Kitavans eat lots of cooked starches could suggest that cooked starches are benign or neutral (perhaps for the Kitavans if not for everyone), but the mere fact of their eating them doesn't guarantee that they're optimal. They clearly aren't essential, since humans wouldn't have survived before cooking otherwise.
-
Where are exactly these studies that show that overfeeding does raise insulin and leptin sensitivity after the overfeeding has ended? Can any study say the sensitivity is still better after even a few months? Theres no way, they have measured this stuff after a year, right? Overfeeding seems like it could be another way to mask symptoms.
There is a study where the Hadza are asked to rank their food choices from best to worst if they were supplied an unlimited supply. Both men and women chose tubers as last. This would be interesting to see what the Kitavans would choose. I don't see how modern potatoes are anything like the Kitavan tubers.
Low carb seems to have completely masked the symptoms of my underlying digestion troubles since I am now doing fairly bad on it.
-
Good points and I would agree that my teeth definitely seemed to become more sensitive when I was including more carbohydrates, especially from cooked starches.
However, like I said, one always has to consider the other variables (leptin) and the potential for the "sticking plaster" effect...The point that I was making is that somewhere along the lines, one must "hit" the carbs to re-develop tolerance and improve sensitivity in the longer term.
My bowel transit time gradually ground to a halt with very low carb, although it massively improved with just the inclusion of cooked starches. The other thing I've noticed is that my body heat (thermogenesis) has dropped since dropping higher carbs and I'm eating fat always to the extent that I get tachycardia (although I just ignore it).
I have innovated an interesting new breakfast though - bananas and custard, although the custard is just 4 egg yolks with a bit of water/coconut oil. I find bananas the easiest way to stay out of ketosis, although I realise that they're prob'ly the least natural of all fruits on the Earth.
I will enumerate some study references forthwith (no time at the moment).
-
Where are exactly these studies that show that overfeeding does raise insulin and leptin sensitivity after the overfeeding has ended? Can any study say the sensitivity is still better after even a few months? Theres no way, they have measured this stuff after a year, right? Overfeeding seems like it could be another way to mask symptoms.
There is a study where the Hadza are asked to rank their food choices from best to worst if they were supplied an unlimited supply. Both men and women chose tubers as last. This would be interesting to see what the Kitavans would choose. I don't see how modern potatoes are anything like the Kitavan tubers.
Low carb seems to have completely masked the symptoms of my underlying digestion troubles since I am now doing fairly bad on it.
So wait, what are you saying? Your digestion is bad now on RPD?
-
On VLC raw paleo...Maybe potassium/electrolytes is a factor though in sluggish bowel transit, as well as bile insufficiency - I don't know yet...
-
Here's another one about rodent endocrinology...
For the first time, terminally ill rodents with type-1 diabetes have been restored to complete health with a single injection of a substance other than insulin.
University of Texas Southwestern (UTS) researchers tested for the first time whether an injection of leptin gene given to insulin-deficient mice dying of diabetic coma could reverse their terminal condition.
. . . . . . .
Could you post a link for that???
-
So wait, what are you saying? Your digestion is bad now on RPD?
I've been raw paleo for 4 months, of which anytime I have gone ZC, bowel movements become very infrequent and at one point extremely painful. They are always badly malformed (extremely thin, etc.). After eating I feel fine and light and nothing like I was when I was on SAD and so I feel like digestion is going smoothly. Even with adding vegetation, stool is very malformed though it isn't painful. Theres a good chance I'm not secreting enough HCL, since I've taken up to 19 HCL pills without feeling any burn after a meal. Recently, the HCL seems to be helping my bowel movement formation. Energy has been pretty low the entire time as well. This is all pointing to the possibility that something is interrupting bile secretion and so I am experimenting with liver flushing. Just did my first one last night with nothing interesting showing up this morning.
-
I have been having some problems as of late aswell.
A lot of constipation which is weird because when I was RZC my bowel movements were excellent. But I have been changing a lot of things lately, one of the changes is I cut out all salt.. And now I've been eating more salt and fruit and I'm bowel movements seem to becoming stable again >_>
-
I'd agree about the biliary insufficiency being the co-factor in low/downregulated stomach acid production.
Given the assumption that biliary debris is orchestrating this less-than-ideal cycle, I've recently been including some cholegogic (bile stimulating) herbal tinctures like yellow dock, bupleurum and dandelion root as part of my main meals - just a small glass of water with 2ml of drops. This definitely seems to better stimulate the digestion, although I doubt that the facilitated uptake reaches anything like optimal.
I think it's short-sighted to dismiss the possibility of minor/major bile occlusion as a pivotal factor in diminished digestive capacity (and ultimately, malnutrition, particularly of fats and fat-soluble things like vitamin A, D and K).
Also, bile is a great lubricant of the stool and stimulator of strong peristalsis...not to mention a major vehicle for fat-soluble toxins leaving the liver. Pretty critical, to my mind...It's like the old adage - not what you intake, but what you uptake...
-
I think it's short-sighted to dismiss the possibility of minor/major bile occlusion as a pivotal factor in diminished digestive capacity (and ultimately, malnutrition, particularly of fats and fat-soluble things like vitamin A, D and K).
I think its possible that nearly every single person that has issues with low-carb has some degree of bile occlusion, which would point to why so many do much better with frankenfoods such as potatoes and yams that are supposedly 'clean' energy - easily digestible with low anti-nutrients and a much lessened need for bile.
-
Another thing I read somewhere recently is that fructose is tenfold more glycating in the presence of PUFA than glucose, although with typical human anatomy, fructose should not enter the general circulation directly because its metabolic pathway includes first the hepatic portal system, then the liver (lipogenesis etc.). However, one may understand that an over-permeable intestine (leaky gut syndrome) may allow passage of fructose into the general circulation, like all of these other weird opioid peptides that can even cross the blood/brain barrier (e.g. casein, gliadin, glutenin etc.). If the fructose can enter the general circulation and contribute to glycation of high-PUFA cell membranes, the result would be inflammation. It's established that inflammation is a factor in insulin resistance disease, so maybe the fructose is a deleterious factor in the equation (as could be glucose, to a lesser extent). It really underscored the point about eliminating all PUFA except the trace amounts in ruminant meat/fat/organs.
One wonders if a starchy or low-fructose fruit (banana, berries etc.) would be more optimal for those recovering from this chaotic interaction of factors in the vicious circle.
This makes me wonder about aajonus' followers who sometimes combine fruit in a meal with chicken or pork, yet never in the same meal with red meat.
Are you implying also berries or bananas might help with carbohydrates because of their B vitamins or type of fiber? What about people who digest non starchy fruit better than starchy ones? Don't people say bananas help sleep? They can help in bone repair and pain.
-
So laughably, lo-carb seems like a sticking plaster (y'know, treating the symptoms rather than underlying cause), possibly while the problem of blunted insulin sensitivity and leptin sensitivity remains.
So how does one treat the underlying symptoms of blunted insulin and leptin sensitivity?
...my teeth definitely seemed to become more sensitive when I was including more carbohydrates, especially from cooked starches.
However, like I said, one always has to consider the other variables (leptin) and the potential for the "sticking plaster" effect...The point that I was making is that somewhere along the lines, one must "hit" the carbs to re-develop tolerance and improve sensitivity in the longer term.
So are you saying that absence of the leptin gene contributes to dental plaque?
My bowel transit time gradually ground to a halt with very low carb, although it massively improved with just the inclusion of cooked starches. The other thing I've noticed is that my body heat (thermogenesis) has dropped since dropping higher carbs and I'm eating fat always to the extent that I get tachycardia (although I just ignore it).
Interesting, I've experienced close to the opposite. My body heat has risen and circulation greatly improved since increasing the fats and decreasing the carbs in my diet. Do you find that cooked carbs help your bowels more than raw fruits?
I have been having some problems as of late aswell.
A lot of constipation which is weird because when I was RZC my bowel movements were excellent. But I have been changing a lot of things lately, one of the changes is I cut out all salt.. And now I've been eating more salt and fruit and I'm bowel movements seem to becoming stable again >_>
Very interesting. Dr. Jay Wortman said his VLC patients resolved constipation when they added salt to their diets. He claimed that VLC diets cause excretion of salt that needs to be offset to avoid constipation. Could this explain how traditional Inuits had very low serum levels of salt despite eating lots of seafood? I've been trying to remember to include salt in my diet but my tolerance for it is pretty low now. This is encouraging, though, so I'll stick with it.
-
^ Maybe try this?
"Mineral salts are utilized by plants for food. We can access them in their bio-available form and in correct concentrations in vegetable juices".
-
Coming from a whole food standpoint, fresh beef blood has salt I think. It may have other nutrients missed to that might work together in a WOE. People say butchers sell blood, especially in ethnic stores, for cooking.
Maybe it comes frozen most of the time.
I was thinking when they (the SAD people) sell toxin laden fatty confinement meat, that much of the toxins melt away with the fat in cooking (rotisserie etc). If they sell blood though, I would imagine it has to be organic or grass raised, as I can't see how toxins would fall out of blood in cooking it. If a majority of people got sick right away from a food, I doubt it would have had an ethnic tradition.
So how does one treat the underlying symptoms of blunted insulin and leptin sensitivity?
So are you saying that absence of the leptin gene contributes to dental plaque?
Interesting, I've experienced close to the opposite. ...Very interesting. Dr. Jay Wortman said his VLC patients resolved constipation when they added salt to their diets. He claimed that VLC diets cause excretion of salt that needs to be offset to avoid constipation. Could this explain how traditional Inuits had very low serum levels of salt despite eating lots of seafood? I've been trying to remember to include salt in my diet but my tolerance for it is pretty low now. This is encouraging, though, so I'll stick with it.
^ Maybe try this?
"Mineral salts are utilized by plants for food. We can access them in their bio-available form and in correct concentrations in vegetable juices".
-
Coming from a whole food standpoint, fresh beef blood has salt I think. It may have other nutrients missed to that might work together in a WOE. People say butchers sell blood, especially in ethnic stores, for cooking.
Maybe it comes frozen most of the time.
I was thinking when they (the SAD people) sell toxin laden fatty confinement meat, that much of the toxins melt away with the fat in cooking (rotisserie etc). If they sell blood though, I would imagine it has to be organic or grass raised, as I can't see how toxins would fall out of blood in cooking it. If a majority of people got sick right away from a food, I doubt it would have had an ethnic tradition.
They sell blood from conventionally raised pigs here. They also make fatty sausages from conventional meat. Also smoked bacon etc., so it's not like people don't consume that kind of fat.
-
Coming from a whole food standpoint, fresh beef blood has salt I think. It may have other nutrients missed to that might work together in a WOE.
The (feedlot?) beef I've bought from local stores drips little blood, while the grass-finished drips a lot, so whatever stays in the meat should provide mineral salts in the most bio-available form.
-
So laughably, lo-carb seems like a sticking plaster (y'know, treating the symptoms rather than underlying cause), possibly while the problem of blunted insulin sensitivity and leptin sensitivity remains.
What's laughable is you looking at one rodent study, then making conclusions about low carb eating. l)
Research done a couple of years ago in St. Louis and in Japan pinpointed the problem. Triglycerides – fat circulating in the blood – interrupts the passage of leptin across the BBB. If trigylcerides are high, which they are in most obese people, then, basically, they block the movement of leptin into the brain. So, leptin levels are elevated in the blood, and triglycerides keep the leptin from getting to where it needs to get to shut off hunger. (click here for the abstract and full text of this research paper.)
We all know that the commonest lab finding in people following a low-carb diet is a dramatic reduction in triglyceride levels. This reduction in triglycerides allows the leptin that is already circulating in relatively large amounts to get through to the brain where it can reduce hunger. I believe that this reduction in triglycerides (which happens fairly quickly) is the primary reason that people substantially decrease their hunger on low-carb diets. And remember from the graphic above that leptin – once it gets to the brain – actually increases thermogenesis as well, which means that the metabolic rate increases.
So, the triglyceride reduction from following a low-carb diet does does double duty when more leptin gets to the brain: hunger goes down and metabolic rate goes up. That duo increases weight loss. Is it any wonder that low-carb diets virtually always manhandle low-fat diets in terms of weight loss in all of the studies in which they are compared? And it it any wonder that when people are allowed to eat an ad lib low-carb diet, they always consume fewer calories than those consuming an ad lib low-fat/high-carbohydrate diet?
http://www.proteinpower.com/drmike/metabolism/leptin-low-carb-and-hunger/
These were done on humans:
221. Eizirik DL, Korbutt GS, and Hellerström C. “Prolonged exposure of human pancreatic islets to high glucose concentrations in vitro impairs the beta-cell function.” Journal of Clinical Investigation, Volume 90, Number 4, Pages 1263–1268. October 1992.http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=443168
222. Frederici M, et al. “High Glucose Causes Apoptosis in Cultured Human Pancreatic Islets of Langerhans.” Diabetes. Volume 50, Number 6, Pages1290-1301, 2001.http://diabetes.diabetesjournals.org/cgi/reprint/50/6/1290
223. Boden G, et al. “Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes.”Annals of Internal Medicine, Volume 142, Number 6, Pages 403-11. March 15, 2005. http://www.annals.org/cgi/content/abstract/142/6/403?etoc
224. Basciano H, Federico L, and Adeli K. “Fructose, insulin resistance, and metabolic dyslipidemia.” Nutrition & Metabolism, (Lond). 2005; Volume 2, Number 5, and online February 21. 2005.http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=552336
225. Maedler K, et al. “Glucose-induced b cell production of IL-1b contributes to glucotoxicity in human pancreatic islets.” Journal of Clinical Investigation, Volume 110, Number 6, Pages 851–860. September 15, 2002.http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=151125
226. Gross LS, Li L, Ford ES, and Liu S. “Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment.” American Journal of Clinical Nutrition, (1,2,3) Volume 79, Number 5, 774-779, May 2004.http://www.ajcn.org/cgi/content/full/79/5/774
227. Gannon MC and Nuttal FQ. “Effect of a High-Protein, Low-Carbohydrate Diet on Blood Glucose Control in People With Type 2 Diabetes.” Diabetes, Volume 53, Number 9, Pages 2375-2382. 2004.http://diabetes.diabetesjournals.org/cgi/content/full/53/9/2375
228. Nuttall FQ and Gannon MC. “The metabolic response to a high-protein, low-carbohydrate diet in men with type 2 iabetes mellitus.” Metabolism. Volume 55, Issue 2, Pages 243-251. February 2006.http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WN4-4J2N7WW-N&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=4ab451c21a4f6af24c243cf0a9325cce
229. Gannon MC and Nuttal FQ. “Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition.” Nutrition and Metabolism. Volume 3, Number 1, Pages 16. 2006.http://www.nutritionandmetabolism.com/content/3/1/16
230. Ruderman N, et al. “The metabolically obese, normal-weight individual revisited.” Diabetes, Volume 47, Number 5, Pages 699-713. May 1988.http://diabetes.diabetesjournals.org/cgi/reprint/47/5/699
231. Freedland ES. “Role of a critical visceral adipose tissue threshold (CVATT) in metabolic syndrome: implications for controlling dietary carbohydrates: a review.” Nutrition & Metabolism, (Lond). Volume Number 12. 2004. Published online November 5. 2004.http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=535537
232. Stratton IM, el al. “Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study.” British Medical Journal (BMJ). Volume 321, Number 7258, Pages 405–412. August 12, 2000.http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=27454
233. Kritchevsky SB and Kritchevsky D. “Egg Consumption and Coronary Heart Disease: An Epidemiologic Overview.” Journal of the American College of Nutrition, Volume 19, Number 90005, 549S-555S (2000).http://www.jacn.org/cgi/content/full/19/suppl_5/549S
234. Arora SK and McFarlane SI. “The case for low carbohydrate diets in diabetes management.” Nutrition & Metabolism, (Lond), 2005; Volume 2, Number 16. 2005. Published online 2005 July 14.http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1188071
235. Nielsen JV and Joensson E. “Low-carbohydrate diet in type 2 diabetes. Stable improvement of bodyweight and glycemic control during 22 months follow-up.” Nutrition & Metabolism, (Lond), Volume 3, Number 22. 2006 Published online June 14, 2006. http://www.nutritionandmetabolism.com/content/3/1/22
236. Agnieszka K. “ISLET AMYLOID - A CULPRIT IN TYPE 2 DIABETES.” The Science Creative Quarterly., Issue 2, September-November 2006.http://www.scq.ubc.ca/?p=274
237. Meyer C, et al. “Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans.” Diabetes Care.Volume 29, Number 8, Pages 1909-14. August 2006. http://care.diabetesjournals.org/cgi/reprint/29/8/1909
238. Lee AT, Reis D and Eriksson UJ. ”Hyperglycemia-induced embryonic dysmorphogenesis correlates with genomic DNA mutation frequency in vitro and in vivo.” Diabetes, Vol 48, Issue 2 371-376.http://diabetes.diabetesjournals.org/cgi/reprint/48/2/371
239. Wentzel P, Ejdesjö A and Eriksson UJ. “Maternal Diabetes In Vivo and High Glucose In Vitro Diminish GAPDH Activity in Rat Embryos.” Diabetes. Volume 52, Number 5, Pages 1222-1228, 2003.http://diabetes.diabetesjournals.org/cgi/reprint/52/5/1222
240. Poitout V, et al. “Chronic Exposure of TC-6 Cells to Supraphysiologic Concentrations of Glucose Decreases Binding of the RIPE3b1 Insulin Gene Transcription Activator.” Journal of Clinical Investigation. Volume 97, Number 4, Pages 1041-1046. February 1996.http://www.jci.org/cgi/reprint/97/4/1041
241. Ahmad N, et al. “Glycated and Oxidized Protein Degradation Products Are Indicators of Fasting and Postprandial Hyperglycemia in Diabetes.”Diabetes Care. Volume 28, Number 10, Pages 2465-2471. 2005.http://care.diabetesjournals.org/cgi/reprint/28/10/2465
242. Schulz M, et al. “Is the Association Between Dietary Glycemic Index and Type 2 Diabetes Modified by Waist Circumference?” Diabetes Care. Volume 29, Number 5, Pages 1102-1104, 2006.http://care.diabetesjournals.org/cgi/reprint/29/5/1102
243. Shaw JE, et al. “Isolated post-challenge hyperglycaemia confirmed as a risk factor for mortality.” Diabetologia. Volume 42, Number 9, Pages 1050-4. September 1999. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10447514&dopt=Abstract
244. Stride A, et al. “Intrauterine Hyperglycemia Is Associated With an Earlier Diagnosis of Diabetes in HNF-1 Gene Mutation Carriers.” Diabetes Care. Volume 25, Number 12, Pages 2287-2291, 2002.http://care.diabetesjournals.org/cgi/reprint/25/12/2287
245. Dabelea D. “The Predisposition to Obesity and Diabetes in Offspring of Diabetic Mothers.” Diabetes Care. Volume 30. Pages S169-S174, 2007.http://care.diabetesjournals.org/cgi/reprint/30/Supplement_2/S169
246. Chari ST, et al. “Probability of Pancreatic Cancer Following Diabetes: A Population-Based Study.” Gastroenterology. Volume 129, Number 2, Pages 504-511. August 2005. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WFX-4GSS016-10&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=ac84cd005cdefd3680962927fdb2df66
247. Tanaka Y, et al. “A role for glutathione peroxidase in protecting pancreatic b cells against oxidative stress in a model of glucose toxicity.” Proceedings of the National Academy of Science of the United States of America. Volume 99, Number 19, Pages 12363–12368. September 17, 2002.http://www.pubmedcentral.gov/articlerender.fcgi?artid=129450
248. Poulaki W. et al. “Acute intensive insulin therapy exacerbates diabetic blood-retinal barrier breakdown via hypoxia-inducible factor-1a and VEGF.”Journal of Clinical Investigation. Volume 109, Number 6, Pages 805–815. March 15, 2002. http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150907
249. Colagiuri S, et al. “Are Lower Fasting Plasma Glucose Levels at Diagnosis of Type 2 Diabetes Associated With Improved Outcomes?” Diabetes Care. Volume 25, Pages 1410-1417, http://care.diabetesjournals.org/cgi/reprint/25/8/1410
250. Stratton IM, et al. “Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study.” British Medical Journal. Volume 321, Number 7258, Pages 405–412. August 12, 2000.http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27454
251. Adler AI, et al. “Association of systolic blood pressure with macrovascular and microvascular complications of type 2 diabetes (UKPDS 36): prospective observational study.” British Medical Journal. Volume 321, Number 7258, Pages 412–419. August 12, 2000.http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=27455&blobtype=pdf
252. Yamamoto T, et al. “Clinical efficacy of insulin-like growth factor-1 in a patient with autoantibodies to insulin receptors: a case report.” Diabetes Research and Clinical Practice. Volume 49, Issue 1, Pages 65-69. July 2000, http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T5Y-408KCG7-9&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=59077bf779760e0c34b30291dee8c5fe
253. Retnakaran R, et al. “Continuous Subcutaneous Insulin Infusion Versus Multiple Daily Injections.” Diabetes Care. Volume 27, Number 11, Pages 2590-2596, 2004.http://care.diabetesjournals.org/cgi/reprint/27/11/2590
254. Lecube A, et al. “Diabetes Is the Main Factor Accounting for the High Ferritin Levels Detected in Chronic Hepatitis C Virus Infection.” Diabetes Care. Volume 27, Number 11, Pages 2669-2675, 2004.http://care.diabetesjournals.org/cgi/content/full/27/11/2669
255. Sheard NF, et al. “Dietary Carbohydrate (Amount and Type) in the Prevention and Management of Diabetes. A statement by the American Diabetes Association.” Diabetes Care. Volume 27, Pages 2266-2271, 2004.http://care.diabetesjournals.org/cgi/content/full/27/9/2266
256. Taylor R, et al. “Direct Assessment of Liver Glycogen Storage by C13Nuclear Magnetic Resonance Spectroscopy and Regulation of Glucose Homeostasis after a Mixed Meal in Normal Subjects.” Journal of Clinical. Investigation. Volume 97, Pages 126–132. January 1996.http://www.jci.org/cgi/reprint/97/1/126
257. Krakoff J, et al. “Comparison of the Effect of Plasma Glucose Concentrations on Microvascular Disease Between Pima Indian Youths and Adults.” Diabetes Care. Volume 24, Number 6, Pages 1023-1028, 2001. http://care.diabetesjournals.org/cgi/reprint/24/6/1023
258. Kilpatrick ED and Robertson RP. “Differentiation Between Glucose-Induced Desensitization of Insulin Secretion and - Cell Exhaustion in the HIT-T15 Cell Line.” DIABETES, Volume 47, Number 4, Pages 606-611. April 1998http://diabetes.diabetesjournals.org/cgi/reprint/47/4/606
259. Robertson RP, et al. “Glucose Toxicity in Beta-Cells: Type 2 Diabetes, Good Radicals Gone Bad, and the Glutathione Connection.” DIABETES. Volume 52, Number 3, Pages 581-587, 2003.http://diabetes.diabetesjournals.org/cgi/reprint/52/3/581
260. Krishnan S, et al. “Glycemic Index, Glycemic Load, and Cereal Fiber Intake and Risk of Type 2 Diabetes in US Black Women.” Archives of Internal Medicine. Volume 167 Number 21, November 26, 2007.http://archinte.ama-assn.org/cgi/content/short/167/21/2304
261. Parillo M, et al. “A high-monounsaturated-fat/low-carbohydrate diet improves peripheral insulin sensitivity in non-insulin-dependent diabetic patients.”Metabolism. Volume 41, Number 12, Pages 373-8. December 1992.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=1461145&dopt=Abstract
262. Colman PG, et al. “Position Statement: New classification and criteria for diagnosis of diabetes mellitus.” Medical Journal of Australia. Volume 170, Pages 375-378. 1999.http://www.mja.com.au/public/issues/apr19/colman/colman.html
263. Brand-Miller JC. “Editorial: Postprandial glycemia, glycemic index, and the prevention of type 2 diabetes.” American Journal of Clinical Nutrition, Volume. 80, Number. 2, Pages 243-244, August 2004.http://www.ajcn.org/cgi/reprint/80/2/243.pdf
264. Bazzano LA, et al. “Prevention of Type 2 Diabetes by Diet and Lifestyle Modification.” Journal of the American College of Nutrition, Volume 24, Number 5, Pages 310–319. 2005.http://www.jacn.org/cgi/content/full/24/5/310
265. Villegas R, et al. “Prospective Study of Dietary Carbohydrates, Glycemic Index, Glycemic Load, and Incidence of Type 2 Diabetes Mellitus in Middle-aged Chinese Women.” Archives of Internal Medicine.. Volume 167 Number 21, Pages 2310-2316. November 26, 2007. http://archinte.ama-assn.org/cgi/content/short/167/21/2310
266. Klein S. “The case of visceral fat: argument for the defense.” Journal of Clinical. Investigation. Volume 113, Number 11, Pages 1530–1532. June 1, 2004. http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=419497&blobtype=pdf
267. Nielsen S, et al. “Splanchnic lipolysis in human obesity.” Journal of Clinical. Investigation. Volume 113, Number 11, Pages 1582–1588. June 1, 2004.http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=419492&blobtype=pdf
268. Haffner SM. “The Importance of Hyperglycemia in the Nonfasting State to the Development of Cardiovascular Disease.” Endocrine Reviews. Volume 19, Number 5, Pages 583–592.http://edrv.endojournals.org/cgi/content/abstract/19/5/583
269. Dorman JS, et al. “Type 1 diabetes in offspring of parents with type 1 diabetes: the tip of an autoimmune iceberg?” Pediatric Diabetes, Volume 1, Number 1, Pages. 17-22. March 2000.http://www.ingentaconnect.com/content/mksg/pdi/2000/00000001/00000001/art00004
270. Boyd AE, 3rd and Moss LG. “When Sugar Is Not So Sweet: Glucose Toxicity.” Journal of Clinical. Investigation. Volume 92, Page 2. July 1993.http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=293513&blobtype=pdf
271. Hirano T and Adachi M. “Insulin-like Growth Factor 1 Therapy for Type B Insulin Resistance.” Annals of Internal Medicine. Volume 127, Issue 3, Pages 245-246. August 1997.http://www.annals.org/cgi/content/full/127/3/245-a\
272. Cavaghan MK, et al. “Interactions between insulin resistance and insulin secretion in the development of glucose intolerance.” Journal of Clinical Investigation. Volume 106, Number 3, Pages 329–333. August 1, 2000.http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=314336&blobtype=pdf
273. King DE, et al. “C-Reactive Protein and Glycemic Control in Adults With Diabetes.” Diabetes Care. Volume 26, Number 5. Pages 1535–1539, 2003.http://care.diabetesjournals.org/cgi/content/full/26/5/1535
274. Skyler JS. “Insulin therapy in type II Diabetes: Who needs it, how much of it, and for how long?” Postgraduate Medicine Online. Volume 101, Number 2. February 1997.http://www.postgradmed.com/issues/1997/02_97/skyler.htm
275. Peyrot M, et al. “Resistance to Insulin Therapy Among Patients and Providers. Results of the cross-national Diabetes Attitudes, Wishes, and Needs (DAWN) study.” Diabetes Care. Volume 28, Pages 2673-2679, 2005.http://care.diabetesjournals.org/cgi/reprint/28/11/2673
276. Wellen KE and Hotamisligil GS. “Inflammation, stress, and diabetes.”Journal of Clinical Investigation. Volume 115, Number 5, Pages1111–1119. May 2, 2005. http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=1087185
277. The Diabetes Prevention Program Research Group. “Intensive Lifestyle Intervention or Metformin on Inflammation and Coagulation in Participants With Impaired Glucose Tolerance.” Diabetes. Volume 54, Number 5, Pages 1566-1572. December 15, 2005.http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=1314967
278. Hundal RS, et al. “Mechanism by which high-dose aspirin improves glucose metabolism in type 2 diabetes.” Journal of Clinical Investigation. Volume 109, Number 10, Pages 1321–1326. May 15, 2002.http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150979
279. Rappaport J and Fonseca V. “Case-Based Study: From Prediabetes to Complications—Opportunities for Prevention.” Peer-reviewed Open Accessed (PLOS) Medicine. Volume 2, Issue 2, Page e40. February 2005.http://medicine.plosjournals.org/perlserv?request=get-document&doi=10.1371/journal.pmed.0020040
280. Shuldiner AR and McLenithan JC. “Genes and pathophysiology of type 2 diabetes: more than just the Randle cycle all over again.” Journal of Clinical Investigation, Volume 114, Number 10, Pages 1414–1417. November 15, 2004. http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=525752
281. Liu,KS, et al. “Insulin-related genes expressed in human placenta from normal and diabetic pregnancies.” Proceedings of the National Academy of Science of the United States of America. Volume 82, Number 11, Pages 3868–3870. June 1985. http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=397889
282. Silverman BL et al. “Long-term effects of the intrauterine environment. The Northwestern University Diabetes in Pregnancy Center.” Diabetes Care, Volume 21, Supplement 2, Pages B142-9. August 1998.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=9704242
283. Hull RL, et al. “Oophorectomy Promotes Islet Amyloid Formation in Human Islet Amyloid Polypeptide Transgenic Mice.” DIABETES, Volume 50, Supplement 1, Pages S184-S185. February 2001.http://diabetes.diabetesjournals.org/cgi/reprint/50/suppl_1/S184.pdf
284. Kahn SE. “CLINICAL REVIEW 135: The Importance of b-Cell Failure in the Development and Progression of Type 2 Diabetes.” Journal of Clinical Endocrinology & Metabolism. Volume 86, Number 9, Pages 4047–4058. 2001. http://jcem.endojournals.org/cgi/reprint/86/9/4047
285. de Rekeneire N, et al. “Diabetes, Hyperglycemia, and inflammation in Older Individuals. The Health, Aging and Body Composition study.” Diabetes Care. Volume 29,Number 8, Pages 1902-1908. 2006.http://care.diabetesjournals.org/cgi/content/full/29/8/1902
286. Parappil A, et al. “Diagnostic criteria for diabetes revisited: making use of combined criteria.” BMC Endocrine Disorders. Volume 2, Number 1. 2002.http://www.biomedcentral.com/1472-6823/2/1
287. Sheard NF, et al. “Dietary Carbohydrate (Amount and Type) in the Prevention and Management of Diabetes. A statement by the American Diabetes Association.” Diabetes Care. Volume 27, Number 9, Pages 2266-2271. 2004. http://care.diabetesjournals.org/cgi/reprint/27/9/2266
288. Resnick HE, et al. “Differential Effects of BMI on Diabetes Risk Among Black and White Americans.” Diabetes Care. Volume 21, Number 11, Pages 1828–1835. November 1998.http://care.diabetesjournals.org/cgi/content/abstract/21/11/1828
289. Sargrad KR, et al. “Effect of high protein vs high carbohydrate intake on insulin sensitivity, body weight, hemoglobin A1c, and blood pressure in patients with type 2 diabetes mellitus.” Journal of the American Dietetic Association. Volume 105, Number 4, Pages 573-80. April 2005.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15800559&itool=iconabstr&query_hl=1
290. Omi H, et al. “Participation of high glucose concentrations in neutrophil adhesion and surface expression of adhesion molecules on cultured human endothelial cells: effect of antidiabetic medicines.” Journal of Diabetes and Its Complications. Volume16, Number 3, Pages 201-8. May-June 2002.http://www.ncbi.nlm.nih.gov/pubmed/12015189?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
291. Allick G, et al. “A Low-Carbohydrate/High-Fat Diet Improves Glucoregulation in Type 2 Diabetes Mellitus by Reducing Postabsorptive Glycogenolysis.” Journal of Clinical Endocrinology & Metabolism . Volume 89, Number 12, Pages 6193-6197. 2004.http://jcem.endojournals.org/cgi/content/full/jcem;89/12/6193
292. Ferrannini E, et al. “Effect of Fatty Acids on Glucose Production and Utilization in Man.” Journal of Clinical Investigation. Volume 72, Pages 1737-1747. November 1983.http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=370462
293. Abdul-Rahman M, et al. “A High-Fat Diet in Obese Patients Induces Weight Loss, Leads to Improved Insulin Resistance, and Lowers Systolic Blood Pressure Despite Marked Increase in Dietary Sodium Intake.” Endocrine Practice. Abstract-Obesity #201. Volume12, Supplement 2, Page 50. 2006.http://www.aace.com/meetings/ams/2006/pdfs/2006AM-Abstracts.pdf
294. Manning PJ, et al. “Changes in Circulating Postprandial Proinflammatory Cytokine Concentrations in Diet-Controlled Type 2 Diabetes and the Effect of Ingested Fat.” Diabetes Care. Volume 27, Pages 2509-2511. 2004.http://care.diabetesjournals.org/cgi/content/full/27/10/2509
295. Hargrove RL, et al. “Low Fat and High Monounsaturated Fat Diets Decrease Human Low Density Lipoprotein Oxidative Susceptibility In Vitro.” Journal of Nutrition. Volume 131, Pages 1758-1763. 2001.http://www.nutrition.org/cgi/content/full/131/6/1758
296. The American College of Endocrinology Task Force on Inpatient Diabetes and Metabolic Control.” American College of Endocrinology Position Statement on Inpatient Diabetes and Metabolic Control.” ENDOCRINE PRACTICE. Volume 10, Number 1, Pages 77-82. January/February 2004.http://www.aace.com/pub/pdf/guidelines/InpatientDiabetesPositionStatement.pdf
297. Xuan S, et al. “Defective insulin secretion in pancreatic ß cells lacking type 1 IGF receptor.” Journal of Clinical Investigation, Volume 110, Number 7, Pages 1011-1019. 2002. http://www.jci.org/110/7/1011?content_type=full
298. THE DIABETES PREVENTION PROGRAM RESEARCH GROUP. “Lipid, Lipoproteins, C-Reactive Protein, and Hemostatic Factors at Baseline in the Diabetes Prevention Program.” Diabetes Care. Volume 28, Number 10, Pages 2472–2479. October 2005.http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=1404506
299. Steinberg HO, et al. “Obesity/Insulin Resistance Is Associated with Endothelial Dysfunction.” Journal of Clinical Investigation, Volume 97, Number 11, Pages 2601-2610. June 1996,http://www.jci.org/97/11/2601/pdf
300. Wright, Jr. E, et al. “Oxidative stress in type 2 diabetes: the role of fasting and postprandial glycaemia.” International Journal of Clinical Practice. Volume 60, Number 3, Pages 308–314. March 2006.http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=1448694
301. Poitout V and Robertson RP. “Minireview: Secondary ß-Cell Failure in Type 2 Diabetes—A Convergence of Glucotoxicity and Lipotoxicity.”Endocrinology. Volume 143, Number 2, Pages 339-342. 2002.http://endo.endojournals.org/cgi/reprint/143/2/339
302. Del Guerra S, et al. “Functional and Molecular Defects of Pancreatic Islets in Human Type 2 Diabetes.” Diabetes. Volume 54, Number 3, Pages 727-735. March 2005. http://diabetes.diabetesjournals.org/cgi/reprint/54/3/727
303. Leibowitz G, et al. “Glucose-Regulated Proinsulin Gene Expression Is Required for Adequate Insulin Production during Chronic Glucose Exposure.” Endocrinology. Volume 143, Number 9, Pages 3214-3220. September 2002. http://endo.endojournals.org/cgi/reprint/143/9/3214
304. Trucco M. “Regeneration of the pancreatic ß cell.” Journal of Clinical Investigation, Volume 115, Number 1, Pages 5-12. January 3, 2005.http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=539206
305. Leibiger, B, et al. “Cell Biology: Short-term regulation of insulin gene transcription by glucose.” Proceedings of the National Academy of Science of the United States of America. Volume 95, Number 16, Pages 9307–9312. August 4, 1998. http://www.pubmedcentral.gov/articlerender.fcgi?artid=21334
306. Parker B, et al. “Effect of a High-Protein, High–Monounsaturated Fat Weight Loss Diet on Glycemic Control and Lipid Levels in Type 2 Diabetes.”Diabetes Care. Volume 25, Number 3, Pages 425-430. March 2002.http://care.diabetesjournals.org/cgi/reprint/25/3/425
307. Nielsen JV, et al. “A low-carbohydrate diet may prevent end-stage renal failure in type 2 diabetes. A case report.” Nutrition & Metabolism (Lond). Volume 3, Number 23. June 14, 2006.http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1523335&blobtype=pdf
308. Miyashita T, et al. “Beneficial effect of low carbohydrate in low calorie diets on visceral fat reduction in type 2 diabetic patients with obesity.” Diabetes Research and Clinical Practice. Volume 65, Number 3, Pages 235-41. September 2004. http://www.cababstractsplus.org/google/abstract.asp?AcNo=20043184309
309. Desai MY. Et al. “Association of Body Mass Index, Metabolic Syndrome, and Leukocyte Count.” American Journal of Cardiology. Volume 97, Issue 6, Pages 835-838. March 15, 2006, http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T10-4J4HJ74-2&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=929bb5cdeabca5440a3b04f30cdb072a
310. Reaven GM. Syndrome X: A Short History.” The Ochsner Journal. Volume 3, Issue 3, Pages 124–125. Summer 2001.http://www.ochsnerjournal.org/perlserv/?request=get-document&issn=1524-5012&Volume=003&issue=03&page=0124&ct=1&SESSID=0747e747edb3d2377ed06d523beb54b3
311. Braga-Basaria M, et al. “Metabolic Syndrome in Men With Prostate Cancer Undergoing Long-Term Androgen-Deprivation Therapy.” Journal of Clinical Oncology. Volume 24, Number 24, Pages 3979-3983. August 20, 2006.http://jco.ascopubs.org/cgi/reprint/24/24/3979
312. Hickey JT, et al. “Clinical Use of a Carbohydrate-Restricted Diet to Treat the Dyslipidemia of the Metabolic Syndrome.” Metabolic Syndrome and Related Disorders. Volume 1, Number 3, Pages 227-232. September 1, 2003. http://www.liebertonline.com/doi/abs/10.1089/154041903322716705?journalCode=met
313. Takano T, et al. “Influences of Statins on Glucose Tolerance in Patients with Type 2 Diabetes Mellitus.” Journal of Atherosclerosis and Thrombosis. Volume 13, Number 2, Pages 95-100. 2006.http://www.jstage.jst.go.jp/article/jat/13/2/95/_pdf
314. Laaksonen DE, et al. “Changes in abdominal subcutaneous fat water content with rapid weight loss and long-term weight maintenance in abdominally obese men and women.” International Journal of Obesity. Volume 27, Pages 677–683. 2003.http://www.nature.com/ijo/journal/v27/n6/full/0802296a.html
http://www.carbohydratescankill.com/
-
http://www.carbohydratescankill.com/
Fantastic book / website.
Something to fawn over.
Thank you!
-
On the original question "Why am I always so tired after eating fruit?"
I only get tired after eating fruit when I eat high fat raw. So the solution to thrive is on days when eating fruit eat only raw lean meat (not together of course). And on days when you want to eat high fat raw don't eat fruit but be zero carb. It's really that simple. But this might not work for people with damaged bodies who are managing symptoms.
FRUIT+RAW LEAN MEAT = BLISS
and
HIGH FAT RAW+RAW LEAN MEAT (zero carb) = BLISS
but
FRUIT+HIGH FAT RAW = TROUBLE
-
Don't people say bananas help sleep?
Bananas are high in Tryptophan, the turkey amino acid that makes one sleepy after meals...this is why bananas for breakfast arn't as get up and go as other things...Typtophan is also important for natural seratonin, the happy chemical...so I guess...go bananas, but they may make you sleepy. Science told me so.
-
Sugar rush. Not enough sugar to make you high, but enough to make you crash afterwards. I have the same thing.
-
This seems like good advice that has been at the back of my mind for a while. What do you base the information on? It's something I'll likely try at some point.
On the original question "Why am I always so tired after eating fruit?"
I only get tired after eating fruit when I eat high fat raw. So the solution to thrive is on days when eating fruit eat only raw lean meat (not together of course). And on days when you want to eat high fat raw don't eat fruit but be zero carb. It's really that simple. But this might not work for people with damaged bodies who are managing symptoms.
FRUIT+RAW LEAN MEAT = BLISS
and
HIGH FAT RAW+RAW LEAN MEAT (zero carb) = BLISS
but
FRUIT+HIGH FAT RAW = TROUBLE
-
I've tried the 30 bananas a day thing for improving my tolerance of fruit. I ate 30-40 bananas a day, meals every 2-3 hours felt best. At first I tried eating every hour, but it didn't agree with my digestion. The first days were terrible, bloating, smelly farts etc. The farts persisted, but they had a neutral smell after some days, and my well-being improved a lot. I stopped after almost two weeks, though, because I became ravenously hungry for meat. As a result, I can now have fruit meals without becoming sleepy afterwards. Like actionhero said, though... not a good idea to combine them with too much fat. And make sure to drink enough water.
-
I just ate an apple and instantly I'm very tired
And it happens almost every time I eat fruit..
So I'm wondering if it's some sort of diabetes or what ever?
Couple of variables and suggestions....
-Some apples are covered with vegetable wax (even organic).
-Ripe fruit digest good for me, over ripe fruit digest the best for me though (maybe it wasn't ripe enough, unripe fruit is harder to digest)
-you can try other fruit (best bet would be in season, local and wild ones)
Edit: well not over ripe (some might take that as almost rotting), just really ripe and really soft is what I do the best on regarding fruit
-
Well local fruit actually may not be the best bet. Since many white people live in the tropics, and some black people live in the arctic.
But that goes back to living in an environment more suited to your genes.