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Old 03-05-2012, 09:21 AM   #181
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Ha ha Peters post made me smile too.

The two things that I earmarked from Dr B 's quotes: no need to consciously limit salt and once goal weight is achieved don't add anything back. I think that is the mistake so many make - reach goal and add back in foods and maintenance is doomed.

I'm happily healthy and maintaining with eggs, meat, and veggies as garnish. I do still use glucomann powder and almond meal mixed together as a thickener or mixed in eggs to make "pancakes". I find my diet to be easy and tasty and my blood glucose levels to be good enough that I still don't need insulin although they are still slightly elevated (I have diabetes after all). Slip from my diet with too much protein or a higher carb veggie and my bgs let me know for 2 days afterwards.
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Old 03-05-2012, 09:29 AM   #182
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Shunsweets, how nice to have you post. You are such an inspiration. Your success is most encouraging.

I like re-reading Dr. B's things. It helps me.
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Old 03-05-2012, 07:41 PM   #183
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Thank you, I needed the laugh! Love Peter. Dr. Bernstein too.
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Old 03-05-2012, 07:43 PM   #184
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Bahahaha! Love hyperlipid!!! Thanks for the link Auntie Em!!
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Old 03-06-2012, 06:27 AM   #185
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Hi, KT and Cathy. Thanks for your kind visits.

I'm going to go look at Peter's post again....

Found this gem in Peter's comments after this post on Physiological Insulin Resistance:

...there is nothing progressive about physiological insulin resistance. You have very little glucose, you divert it to your brain. If you allowed yourself more glucose you would make more insulin, reduce fatty acid release from adipocytes and increase your insulin sensitivity to an appropriate level. Might take a few days.

The problem with pathological insulin resistance appears to come from your adipocytes becoming insulin resistant, probably through over distention with triglycerides, and then releasing palmitic acid even in the presence of as much insulin as your pancreas can produce. They probably got that over distended due to hyperinsulinaemia being used to mop up glucose released by your insulin resistant liver. Your liver gets insulin resistant through fructose. Which means sucrose and HFCS.

The messenger is the same. One is normal physiology, the other is fructose poisoning. That's ignoring issues like bisphenyl A in your fat cells, which probably matters. There is probably an issue with mitochondrial dysfunction in adipocytes which is a trigger for insulin resistance and inappropriate free fatty acid release too.

So on chicken and coconut you would use free fatty acids to keep glucose out of muscles and available for brain, you really would die without this phenomenon. You would not usually become hyperglycaemic, though I know of one person who has achieved this in extreme ketosis for difficult weight loss. A few carbs sorted this out....
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Last edited by Auntie Em; 03-06-2012 at 06:59 AM.. Reason: added information
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Old 03-06-2012, 09:23 AM   #186
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More from Dr. B on why small numbers are important, from an article at the Nutrition and Metabolism Society. I underlined parts of the excerpt.

Why is a low CHO diet essential? We herein ignore the fact that dietary protein
(3) also affects BG and must be covered by much smaller amounts of insulin than the
same weight of CHO.

Consider first the usual attempts to precisely cover ingested CHO
with insulin. Let’s assume that one unit of crystalline insulin will cover exactly 8 gm of
oral CHO for a particular patient. She would inject 12 ½ units to cover a 100 gm CHO
meal.

The food labeling requirements in the USA permit an error of plus or minus 20%
for any ingredient including CHO.

Thus, if the product (say pasta) were underestimated
on the label by 20%
and if one gm CHO would raise her BG by 5 mg/dl, her anticipated
BG would be overestimated by 20 gm x 5 mg/dl or 100 mg/dl --- ergo hypoglycemia
would occur if her target was less than 150 mg/dl. When eating one tenth of this amount of CHO, the uncertainty in BG would only be 10 mg/dl and hypoglycemia would be prevented.

Last edited by Auntie Em; 03-06-2012 at 09:26 AM.. Reason: underlining
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Old 03-06-2012, 01:43 PM   #187
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I started a thread in the Weight Loss Journals, in case anyone would like to look at it. I have never cared too much for reading recipes and menus in this thread.

VLC on a budget as ancestral as I can make it

Best wishes to all for a lovely evening.
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Old 03-09-2012, 07:44 AM   #188
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Circulating glucose levels modulate desire for high-calorie foods in humans, article at the Journal of Clinical Investigation.

An excerpt:

We conclude that the glycemic state modulates the complex interplay between the PFC and hypothalamic and mesolimbic neural control of food-seeking behavior. Transient modest reductions in circulating glucose decrease prefrontal cortical inhibitory control and could promote overeating, particularly in an environment inundated with visual cues of high-calorie foods. These data imply that strategies to minimize postprandial decrements in glucose, including consumption of smaller, more frequent meals, may be helpful in reducing the risk of overeating high-calorie foods, particularly in obese individuals.
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Old 03-09-2012, 03:54 PM   #189
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I haven't gotten through all the science yet, but Chris Masterjohn has given an explanation of how our bodies can make sugar from fat:

The Daily Lipid: We Really Can Make Glucose From Fatty Acids After All! O Textbook, How Thy Biochemistry Hast Deceived Me!

Barry Groves has an article at his site, from Prof. John Yudkin on why low-carb diets must be high fat, not high protein. Chris Masterjohn's post sheds much light on this subject.

So many, even Dr. B, say that fat doesn't not raise blood sugar. I am wondering, if there are particular malfunctions, as well as the Chinese Restaurant effect, which might activate the process Chris explains.

Here is the excerpt from Prof. Yudkin's article:

Which source of base material is best?

The question now, in this era of dietary plenty, is: Which source is healthiest? There are three possible choices:

Glucose, which comes mainly from carbohydrates, although protein can also be utilised as a glucose source by the body if necessary;
Fats, both from the diet and from stored body fats;
Ketones which are derived from the metabolism of fats

Not all cells in our bodies use the same fuel.
Cells that can employ fatty acids are those that contain many mitochondria: heart muscle cells, for example. These cells can make energy from fatty acids, glucose, and ketones, but given a choice, they much prefer to use fats.
Cells that cannot use fats must use glucose and/or ketones, and will shift to preferentially use ketones. These cells also contain mitochondria.
But we also have some cells that contain few or no mitochondria. Examples of cells with few mitochndria are white blood cells, testes and inner parts of the kidneys; and cells which contain no mitochondria are red blood cells, and the retina, lens and cornea in the eyes. These are entirely dependent on glucose and must still be sustained by glucose.

This means that when we limit carb intake, the same energy sources must be used, but a greater amount of energy must be derived from fatty acids and the ketones derived from fatty acids, and less energy from glucose.



Sources of glucose

To understand how a low carb diet works, we need to look at how we eat. This process is one of eating, digestion, hunger and eating again. During our evolution, we also must have experienced long periods when food was in short supply and we starved. This is a pattern our bodies are adapted to. And they have developed mechanisms to cope with a wide range of circumstances. Firstly, the human body must contain adequate levels of energy to sustain the essential body parts that rely on glucose. The brain and central nervous system may be a particular case as, although the brain represents only a small percentage of body weight, it uses between twenty and fifty percent of all the resting energy used by the body.[ii] Fortunately the brain can also use ketone bodies derived from fats. During fasting in humans, and when we are short of food, blood glucose levels are maintained by the breakdown of glycogen in liver and muscle and by the production of glucose primarily from the breakdown of muscle proteins in a process called gluconeogenesis, which literally means 'glucose new birth'.[iii]

But we don't want to use lean muscle tissue in this way: it weakens us. We want to get the glucose our bodies need from what we eat. Some of that will come from carbs, the rest from dietary proteins. Our bodies need a constant supply of protein to sustain a healthy structure. This requires a fairly minimal amount of protein: about 1 to 1.5 grams per kilogram of lean body weight per day is all that is necessary to preserve muscle mass.[iv] Any protein over and above this amount can be used as a source of glucose.

Dietary proteins are converted to glucose at about fifty-eight percent efficiency, so approximately 100g of protein can produce 58g of glucose via gluconeogenesis.[v] During prolonged fasting, glycerol released from the breakdown of triglycerides in body fat may account for nearly twenty percent of gluconeogenesis.[vi] Body fats are stored as triglycerides, molecules that contain three fatty acids combined with glycerol. The fatty acids are used directly as a fuel, with the glycerol stripped off. This is not wasted. As the glycerol is nearly ten percent of triglyceride by weight and two molecules of glycerol combine to form one molecule of glucose, this also supplies a source of glucose.



In some parallel life, I am a biochemist and understand these things.

Thought I'd post this, in case someone else finds these things fascinating....

Best wishes to all.

Last edited by Auntie Em; 03-09-2012 at 03:58 PM..
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Old 03-10-2012, 09:54 AM   #190
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Wow reading this one really took me back to my advanced biochemistry classes and memorizing the Krebs cycle. So now acetone can be processed into pyruvate after all and the process is probably regulated by insulin levels. Fascinating stuff. I'm trying to wrap my mind around the dietary implications of this for my insulin deficient diabetes and high fat/vlc diet. It seems it is more an explanation of causality rather than requiring any dietary change except to note that the body will make what it needs from the nutrients on hand including making the small amount of essential glucose from fats if carbs and proteins are not sufficient. I think this is a good thing as no one wants to deprive their retinas, red blood cells, or immune system of the glucose they require.

I'm a science nerd too AuntieEm and enjoy reflecting on these biochemical interactions. Thanks for the post.

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Old 03-10-2012, 10:13 AM   #191
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Oh, Shunsweets, what a useful thing to have studied! Thanks so much for your post!

Do you mind a question? Can you say if this now proves that Dr. Alfred Pennington was right about the pyruvic acid?

Treatment of OBESITY with Calorically UNRESTRICTED DIETS

I'm not very good at copying text from a pdf. Using a search for "pyruvic" will show the section which was central to Dr. Pennington's theory.

Here are the search results for "pyruvic" in Dr. Blake Donaldson's references to Dr. Pennington's work, in Strong Medicine:

HathiTrust Digital Library Search Inside - Strong medicine.


And in Dr. Richard MacKarness', Eat Fat and Grow Slim, he also refers to Dr. Pennington's findings about pyruvic acid.

Mr. Fatten-Easily's trouble is thought to be his inability to oxidise pyruvic acid properly - the so called pyruvic acid block.

He gets stuck with large quantities of pyruvic acid which is bad for him in two ways:

He cannot readily use it for energy, so he takes it by a short cut to his fat stores.

It prevents the mobilisation of fat from his fat stores by inhibiting the oxidation of fatty acids.

If a fat man stops eating carbohydrate, he makes little pyruvic acid and removes the stimulus to his "fat organ" to make fat.

By eating fat and protein he bypasses his metabolic block.

To put it another way: obesity may be regarded as a compensatory overgrowth of the fatty tissues providing for an increased use of fat by a body incapable of using carbohydrate properly.

Feed a fat man fat and protein in place of starch and sugar and he will deal with that quite well, drawing on his stores of body fat in the process.

Paradoxically, he will eat fat and grow thinner.

He will also feel well because he will no longer be subjecting his body to starvation and he will be tackling the fundamental cause of his obesity which is not overeating but a defect in the complex biochemical machinery of his body.


...

Weight would then be gained on quite a small intake of carbohydrate food because most of it was being diverted into storage and prevented from being got out again for use.

This is what seems to happen in the obese and a possible cause is the pyruvic acid or some such block on the normal metabolic pathway from carbohydrate to energy and from stored fat to energy.



...


Another great advantage of the diet is that it will not take your weight below normal for your height and build, nor will it do you any harm if you only want to lose a few pounds.

But if this is the case, it will not be necessary to restrict carbohydrate to the minimum, but merely to cut it down to a level where the amount of pyruvic acid (which is preventing you mobilising your fat) in your body is reduced to a level at which you can lose weight. This level can be found by trial and error.

As Dr. Pennington puts it:

"It seems that the emphasis should be put on fat as a major source of energy, with carbohydrate restricted to the degree necessitated by the obesity defect, and ample protein allowed for its well recognised benefits to health."

Last edited by Auntie Em; 03-10-2012 at 10:22 AM.. Reason: typing error
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Old 03-11-2012, 09:30 AM   #192
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I think it is well accepted science that pyruvate or pyruvic acid in the body blocks the oxidation of fat. Similar to the way high insulin levels turn off fat burning and put the body in fat storage mode. The pyruvate studies were earlier than the insulin studies but the two are interlinked biochemically.

So looking at Pennington, Donaldson, and Mackarness' discussions on pyruvic acid they are all correct and their theories supported by these newer studies. Of course the new studies were focused on the role of fats and their ability to be used to produce glucose but the same studies reinforce that the pyruvic acid does act in the way the earlier lc diet gurus thought. I love it when intelligent pioneers are found to be correct in their theories by modern research. At least that is how I am interpreting these results.

Seems high fat/lc /moderate protein as a dietary choice, particularly for those with metabolic syndrome or diabetes, is the way to go.
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Old 03-11-2012, 09:58 AM   #193
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Shunsweets, thanks very much! Do you know why there was such a backlash at Dr. Pennington's saying it was the pyruvic acid?

Yes, to the lc:hf:mp as a lifetime choice. For some of us, that is it.

Do you have to make special adjustments to keep your blood sugar normal and constant, if you don't mind the question?
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Old 03-11-2012, 02:21 PM   #194
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I'm not sure why Pennington's peers were so critical of his findings but seeing what happens with the current controversies in the diet community I am not surprised.

I have to make constant adjustments to try to maintain my bgs within my goal range of <100 fasting and <140 post prandial ( and these are very generous ranges - Dr B would like all diabetics to average 83 at all times - I can't manage that without insulin and I am not ready to go there yet for multiple reasons). My bgs also react to stress, exercise, and especially to my food allergies so it can be a definite balancing act. I've been working for nearly 3 years to find the best diet and strategies and still constantly adjust.
I also take metformin and a few selected supplements.
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Old 03-12-2012, 06:33 AM   #195
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Shunsweets, thanks so much for your post. Do you take Biotin, EPO, Magnesium, ALA or R-ALA or other supplements to help control blood sugar? Are you happy with how the Metformin does? I got Dr. B's new book, and the part about graded, progressive exercise jumped out at me, more than it ever had. I realized I could increase exertion and improve mitochondrial health within my own parameters. Jumping more on the rebounder, walking up hills more.

Do you find that allergic reactions raise blood sugar levels?

This is such an endless puzzle, I find. Yes, reading, adjusting, seeing what helps, and how much.

I don't remember who it was that was so dismissive of Dr. Pennington's finding about pyruvic acid. (I'd guess that Ancel Keys was in the dismissive crowd....)

As you said, it's a dear relief to see that the early pioneers are being vindicated.

I really appreciate your posts. Thanks very much!
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Old 03-13-2012, 08:01 AM   #196
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Dr. Jay Wortman has a new post up at his blog about LCHF being not only for weight loss. Here is most of the text:



... So far, as I see it, the whole argument revolves around what causes obesity. While I agree that obesity is a big problem and that there must be some kind of valid explanation for why this epidemic has taken off over a few recent decades, what is missing is recognition that it’s not just about weight. The weight gain is associated with other chronic conditions which are actually the real issue. The current paradigm implies that weight gain is a causal link in the chain that connects to diabetes, cardiovascular disease and a host of other common conditions. I think that weight gain is not, in and of itself, causal. It is another of the conditions that are symptomatic of the underlying cause which is related to carbohydrates in the diet. The fact that you can have thin people develop hypertension, diabetes and heart disease suggests that weight gain is not causal. The fact that you can have obese people with normal cardiometabolic markers and outcomes reinforces this observation. So, when it comes to applying a therapy that is effective in offsetting the harms associated with weight gain (note I said “associated with”, not “caused by”) it is important to address the actual underlying cause. The evidence supporting the highly effective therapeutic use of LCHF diet for these conditions reinforces the idea that dietary carbohydrates are, in fact, the cause. Perhaps we need to add the qualifier, “in susceptible people”. In any case, clinicians who use this approach report remarkable results that go beyond the effectiveness of the usual drug based therapies. It all hinges, of course, on compliance.

The benefits of LCHF actually extend into other realms of pathology that have been hitherto unexplored in terms of a potential dietary cause. I have collected a few anecdotal reports of the kinds of things that continually amaze me when it comes to the benefits of LCHF.

Arthritis

A few years ago, after I had just figured out that a LCHF diet had fixed my own diabetes and metabolic syndrome, I began to speak out about its potential benefits for others. At the time, I was the Regional Director of the Pacific Region of First Nations and Inuit Health Branch of Health Canada. I was asked to speak at an annual meeting of the nurses who worked in rural and remote First Nations communities so I gave a talk about my experiences in reducing carbs and proposed that it might be useful for the management of their diabetic patients. After the meeting ended, I was approached by a nurse who told me a remarkable story. She was caring for a First Nations woman who had severe, debilitating osteoarthritis. The disease was so severe that the woman could not get off a chair without assistance. The woman was overweight so, for whatever reason, the nurses put her on the Atkins diet. After an initial weight loss of a few pounds, the woman relapsed and regained the weight and then tried the diet again. What was remarkable about this was that, as soon as the diet was started the arthritic pain virtually vanished. It returned when the diet was discontinued and vanished again as soon as it was re-started. Clearly this amazing recovery was not associated with weight loss, but rather was directly attributable to the diet. Later, when I met with Dr Eric Westman for the first time, one of the questions I asked was whether he had seen anything like this in his patients. He said he had. I have since heard similar case reports from others who use LCHF diets in their research or clinical practices. So far, I am not aware of a study that has looked at this specific finding but I continue to hear anecdotal stories of this kind of benefit from LCHF.

Milroy’s Syndrome

When we did the trial in Alert Bay, one of the subjects was a man who suffered from Milroy’s syndrome. This is a rare condition where the lymph system malfunctions and fluid accumulates, usually in the lower limbs. The only treatments are mechanical massaging to force the fluid out and the use of devices such as support hose to minimize the accumulation of fluid. In this man’s case, the condition had progressed to the point where he didn’t want to be seen in shorts because of the disfiguring swelling of this legs. After a few months on the LCHF study diet, his condition had almost completely resolved.

Hemochromatosis

Recently, I was contacted by a physician who has implemented a successful diet program in the small village in which he practices. We have been collaborating in an effort to ensure that the considerable weight loss achievements of his patients is sustainable over the long haul by re-introducing fats into their diets once they reach their weight loss targets. He has more recently been starting people on a LCHF diet at the outset. He contacted me to share the details of a woman who he was treating for hemochromatosis. This is a pathological condition where the body has excess iron stores. Left unchecked it can damage major organs and leads to other serious diseases including diabetes, cirrhosis, cardiomyopathy and arthritis. The most effective treatment is phlebotomy, ie blood letting. The woman he was treating was in constant pain and needed phlebotomy every 2 to 4 weeks. After she started the Atkins diet, she went into remission. The pain went away and she no longer needed phlebotomy. She relapsed on the diet and the pain and hemochromatosis returned. After some more phlebotomies, she re-started the diet and has been symptom free and has required no phlebotomies now for the past eight months.

Crohn’s Disease

I received a recent update from another successful diet project that I have been assisting in another small community. The results are pretty good for weight loss but, again, the most remarkable story is about a different condition. In this case it is Crohn’s disease. This is a very debilitating inflammatory condition of the bowel that makes life miserable for the sufferer and which is treated with a variety of drug and surgical interventions. There is no cure. A woman who had suffered from Crohn’s for twelve years went into complete remission after switching to a LCHF diet. Her symptoms completely resolved and her most recent endoscopy found no signs of the disease. She apparently cried upon hearing those results. I can understand why.



Obviously these are just case reports and more research would be needed to verify that these and possibly other conditions can be treated or cured by switching to a LCHF diet and to rule out other possible confounding factors. For the time being, however, those who suffer from these conditions should be encouraged to try the diet. As we now know, there is no downside and the potential upside could be seriously life-altering.

LCHF is about so much more than just weight loss. Eventually the research will be done to explore these other benefits. In the meantime, these squabbles about the various arcane explanations for weight gain that overlook both the well-documented and the anecdotal accounts of the other benefits of LCHF are seriously missing the mark. The proof is in the LCHF pudding, IMHO. And, as you can see from the photos of what I eat in earlier posts, you would have to agree that there is no shortage of “food reward” in the LCHF diet that I follow.
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Old 03-13-2012, 09:22 AM   #197
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Hi AuntieEm. Interesting post. I have seen the high fat ketogenic diet used clinically for epileptic children and the results are amazing in most cases so I do think many health problems respond to this diet as Wortman reports. I like as many confirmations as possible that what I am doing is healthy and beneficial so thanks again.

I did use EPO and R-ALA for a few months right after my dx with diabetes. Didn't see any measurable results in my bgs. I still take fish oil, CLO, magnesium, biotin, a multivit, K+, and melatonin for sleep. I am not sure if any are really helping bgs but I feel good with these supplements. I just started a trial of beta glucan to see if it helps with allergies. I also have to take benadryl most nights to prevent hives and itchiness.
Metformin doesn't make a huge difference in my bgs - about 10-15 pts but it does seem to curb my appetite and make it much easier to stay vlc/hf. Weight is not a problem for me but I used to have a lot more cravings for carbs prior to the met. Maybe it helps my cells get the nourishment they need and they stop sending out the constant hunger signals.
I find allergic reactions and any inflammatory responses do send bgs up as well as any illness. I just try to deal with those as they occur. Diabetes is a constant balancing act.
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Old 03-13-2012, 09:31 AM   #198
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Shunsweets, thanks so much for your kind thoughts and very helpful post. I, too, feel reassured, reading reports of LCHF helping serious health challenges.

I take what you do, except for K and melatonin. Are you taking the K2 from Thorne? I've heard from several folks that they think it is the best on the market. I hope the beta glucans helps you. To have to take diphenhydramine each night is hard. I only do that during the worst of the pollen season or if something seems like an allergy symptom. I also take Evening Primrose Oil, and E, for generally feeling better, and was glad to read in Dr. B's newest book, that those help w/ blood sugar control. Am also taking digestive enzymes to try to get more use out of my food. I started L-Carnitine/ALA recently, and find it really helps with feeling alert and thinking clearly.

I'm glad the Metformin helps. I've heard from others that it helps with staying LC and keeping weight off.

Thanks again for your kind post.

Hope your day is especially lovely.
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Old 03-14-2012, 02:05 PM   #199
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Read this list at WAPF on a diet for pregnant and nursing mothers, thought it noteworthy:


Cod Liver Oil to supply 20,000 IU vitamin A and 2000 IU vitamin D per day

1 quart (or 32 ounces) whole milk daily, preferably raw and from pasture-fed cows

4 tablespoons butter daily, preferably from pasture-fed cows

2 or more eggs daily, preferably from pastured chickens
Additional egg yolks daily, added to smoothies, salad dressings, scrambled eggs, etc.

3-4 ounces fresh liver, once or twice per week (If you have been told to avoid liver for fear of getting "too much Vitamin A," be sure to read Vitamin A Saga)

Fresh seafood, 2-4 times per week, particularly wild salmon, shellfish and fish eggs

Fresh beef or lamb daily, always consumed with the fat

Oily fish or lard daily, for vitamin D

2 tablespoons coconut oil daily, used in cooking or smoothies, etc.

Lacto-fermented condiments and beverages

Bone broths used in soups, stews and sauces

Soaked whole grains [of course the non-WAPFers avoid these }]

Fresh vegetables and fruits

AVOID:
Trans fatty acids (e.g., hydrogenated oils)
Junk foods
Commercial fried foods
Sugar
White flour
Soft drinks
Caffeine
Alcohol
Cigarettes
Drugs (even prescription drugs)
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Old 03-15-2012, 09:57 AM   #200
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More about glucose, ketones, and metabolism, explaining what that pyruvic acid is for:

Introduction to Metabolism. The Black Box of Life. « Richard David Feinman
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Old 03-19-2012, 11:51 AM   #201
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Auntie Em, that is probably the best site I've had the pleasure of perusing in years.
Thanks.
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Old 03-20-2012, 07:33 AM   #202
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Hi, Jem. I'm glad you like it. Hope you are doing really well.
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Old 03-20-2012, 08:15 AM   #203
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It is nice to see peop forging ahead in the world of reseach re LC.

I have to agree that it is a waste of time defending and constantly going back to very old small studies....like the Inuit, for instance.
That is such a different time and place. Also peop today want to see blood work, bone scans, BG's, etc.

Showing current results from peop living in THIS world are what is going to make a difference.
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Old 03-20-2012, 08:21 AM   #204
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Jem, thanks for posting that. I agree, how LC helps us now, with test results.

Ran across this paper on the relatedness of diabetes, obesity and dementia, and LC,

Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet

http://www.lizscript.co.uk/glyn/EJIM01.pdf

Their "Learning Points" list, at the end of the article:

• The amyloid-β present in Alzheimer's plaque may not be causal,
since drug-induced suppression of its synthesis led to further cognitive decline in the controlled studies performed so far.
• Researchers have identified mitochondrial dysfunction and brain insulin resistance as early indicators of Alzheimer's disease.
• ApoE-4 is a risk factor for Alzheimer's disease, and ApoE is involved in the transport of cholesterol and fats, which are essential for signal transduction and protection from oxidative damage.
• The cerebrospinal fluid of Alzheimer's brains is deficient in fats and cholesterol.
• Advanced glycation end-products (AGEs) are present in significant amounts in Alzheimer's brains.
• Fructose, an increasingly pervasive sweetening agent, is ten times as reactive as glucose in inducing AGEs.
• Astrocytes play an important role in providing fat and cholesterol to neurons.
• Glycation damage interferes with the LDL-mediated delivery of fats and cholesterol to astrocytes, and therefore, indirectly, to neurons.
• ApoE induces synthesis of Aβ when lipid supply is deficient.
• Aβ redirects neuron metabolism towards other substrates besides glucose, by interfering with glucose and oxygen supply and increasing bioavailability of lactate and ketone bodies.
• Synthesis of the neurotransmitter, glutamate, is increased when cholesterol is deficient, and glutamate is a potent oxidizing agent.
• Over time, neurons become severely damaged due to chronic exposure to glucose and oxidizing agents, and are programmed for apoptosis due to highly impaired function.
• Once sufficiently many neurons are destroyed, cognitive decline is manifested.
• Simple dietary modification, towards fewer highly-processed carbohydrates and relatively more fats and cholesterol, is likely a protective measure against Alzheimer's disease.

Last edited by Auntie Em; 03-20-2012 at 08:22 AM.. Reason: added title
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Old 03-21-2012, 08:02 AM   #205
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On the effect of ketogenic diets on the brain:

It was a study on mice, but, nevertheless, interesting:

Response of brain amino acid metabolism to ket... [Neurochem Int. 2005] - PubMed - NCBI


Neurochem Int. 2005 Jul;47(1-2):119-28.
Response of brain amino acid metabolism to ketosis.
Yudkoff M, Daikhin Y, Nissim I, Horyn O, Lazarow A, Luhovyy B, Wehrli S, Nissim I.
Source
Department of Pediatrics, University of Pennsylvania School of Medicine, Children's Hospital of Philadelphia, 34th Street and Civic Center Boulevard, Philadelphia, PA 19104, USA.
Abstract
Our objective was to study brain amino acid metabolism in response to ketosis. The underlying hypothesis is that ketosis is associated with a fundamental change of brain amino acid handling and that this alteration is a factor in the anti-epileptic effect of the ketogenic diet. Specifically, we hypothesize that brain converts ketone bodies to acetyl-CoA and that this results in increased flux through the citrate synthetase reaction. As a result, oxaloacetate is consumed and is less available to the aspartate aminotransferase reaction; therefore, less glutamate is converted to aspartate and relatively more glutamate becomes available to the glutamine synthetase and glutamate decarboxylase reactions. We found in a mouse model of ketosis that the concentration of forebrain aspartate was diminished but the concentration of acetyl-CoA was increased. Studies of the incorporation of 13C into glutamate and glutamine with either [1-(13)C]glucose or [2-(13)C]acetate as precursor showed that ketotic brain metabolized relatively less glucose and relatively more acetate. When the ketotic mice were administered both acetate and a nitrogen donor, such as alanine or leucine, they manifested an increased forebrain concentration of glutamine and GABA. These findings supported the hypothesis that in ketosis there is greater production of acetyl-CoA and a consequent alteration in the equilibrium of the aspartate aminotransferase reaction that results in diminished aspartate production and potentially enhanced synthesis of glutamine and GABA.


And another:

The ketogenic diet influences the levels of exc... [Epilepsy Res. 2005] - PubMed - NCBI

Epilepsy Res. 2005 May;64(3):115-25.
The ketogenic diet influences the levels of excitatory and inhibitory amino acids in the CSF in children with refractory epilepsy.
Dahlin M, Elfving A, Ungerstedt U, Amark P.
Source
Department of Pediatrics, Astrid Lindgren Children's Hospital, Karolinska Hospital, SE-171 76 Stockholm, Sweden. maria.dahlin@karolinska.se
Abstract
The ketogenic diet (KD) is an established treatment for medically refractory pediatric epilepsy. Its anticonvulsant mechanism is still unclear. We examined the influence of the KD on the CSF levels of excitatory and inhibitory amino acids in 26 children (mean age 6.1 years) with refractory epilepsy. Seventeen amino acids were determined before and at a mean of 4 months after the start of the KD. Seizures were quantified. Highly significant changes were found in eight amino acids: increases in GABA, taurine, serine, and glycine and decreases in asparagine, alanine, tyrosine and phenylalanine. However, aspartate, glutamate, arginine, threonine, citrulline, leucine, isoleucine and valine/methionine remained unchanged. A significant correlation with seizure response was found for threonine (P=0.016). The GABA levels were higher in responders (>50% seizure reduction) than in nonresponders during the diet (P=0.041). In the very good responders (>90% seizure reduction), the GABA levels were significantly higher at baseline as well as during the diet. Age differences were found with significantly larger decreases in glutamate and increases in GABA in connection with the diet in younger children. Our results indicate that the KD significantly alters the levels of several CSF amino acids that may be involved in its mechanism of action and the increase in GABA is of particular interest.



And one more:

The ketogenic diet may have mood-stabilizing ... [Med Hypotheses. 2001] - PubMed - NCBI

The ketogenic diet may have mood-stabilizing properties.
El-Mallakh RS, Paskitti ME.
Source
Department of Psychiatry and Behavioral Sciences, University of Louisville School of Medicine, Kentucky 40292, USA.
Abstract
The ketogenic diet, originally introduced in the 1920s, has been undergoing a recent resurgence as an adjunctive treatment for refractory epilepsy, particularly in children. In this difficult-to-treat population, the diet exhibits remarkable efficacy with two-thirds showing significant reduction in seizure frequency and one-third becoming nearly seizure-free. There are several reasons to suspect that the ketogenic diet may also have utility as a mood stabilizer in bipolar illness. These include the observation that several anticonvulsant interventions may improve outcome in mood disorders. Furthermore, beneficial changes in brain-energy profile are noted in subjects on the ketogenic diet. This is important since global cerebral hypometabolism is a characteristic of the brains of depressed or manic individuals. Finally, the extracellular changes that occur in ketosis would be expected to decrease intracellular sodium concentrations, a common property of all effective mood stabilizers. Trials of the ketogenic diet in relapse prevention of bipolar mood episodes are warranted.


Emma had this to say about what ketosis does to the brain, at her blog for those on the FailSafe diet:

http://autoimmunethyroid.wordpress.c...to-the-brain/:

Glutamate and aspartate are both ‘bad’ neurotransmitters for people with food chemical intolerance (aspartate is involved in salicylate reactions on NMDA receptors). Ketosis appears to reduce aspartate levels by moving glutamate production away from aspartate and towards GABA and glutamine. Other glutamate-opposing amino acids like taurine, serine and glycine are raised too. GABA and glutamine are both ‘good’, calming neurotransmitters for failsafers.
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Old 03-24-2012, 08:36 AM   #206
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I haven't been around much lately, but I'm still eating right and maintaining my weight.

I referred earlier in this thread to a girlfriend bringing me a 12 pack of Budweiser as a gift and our subsequent discussions.

Well, on Thursday, March 22, that girlfriend became my wife. We have moved her houseful of furniture together with my houseful and are in the midst of sorting it all out. We make daily trips to Goodwill.

I'm very happy and believe my diet has played a big part in my present happy
life.
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Old 03-24-2012, 10:41 AM   #207
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Love to hear this Ron. Congratulations to you and best wishes to your soul mate!!
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Old 03-24-2012, 04:56 PM   #208
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Wonderful news Ron! Much happiness to you both.
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Old 03-24-2012, 10:38 PM   #209
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I am so happy for you, Ron!!!
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Old 03-26-2012, 12:44 PM   #210
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Wow, Ron, either time flies or that was a whirlwind. Congrats!!
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