This page summarizes some of the science behind low carb / paleo diets:
The science of low carb
It takes a lot more exercise and probably some anabolic steroids?
The only thing that ordinary people do get is better strenght and a better fysical capability.. verry seldom a real muscle growht!
There's tons of websites and blogs for low-carb and ketosis. My favorite, the one I visit most often, is lowcarb.ca. In fact, that's where I heard about Andreas Eenfeldt and LCHF in Sweden, and basically all other websites and blogs about low-carb I visit. It's primarily a forum, but there's also tons of info about studies, history of low-carb, etc. If you visit the lowcarb.ca forum, be sure to check out the media/research sub-forum. That's where all the current news about low-carb is posted. You can also check out the various sub-forums dedicated to specific diets like Atkins, Protein Power, etc. Even if you don't visit that forum, this here is one of the top low-carb blogs in my opinion. You're already in the right place.
Gout is not related to red meat, nor any kind of meat, nor protein. It's caused by sugar, most likely fructose. It's also caused or at least exacerbated by alcohol. Look up fructose metabolism, and you'll find out all about gout. It's also strongly associated with diseases caused by carbohydrate poisoning; obesity, diabetes, hypertension.
I understand the hypothesis that says an amino acid - purine - can convert to uric acid, which can then lead to gout. But the problem with this hypothesis is that gout occurs independently of uric acid blood level. You can have low uric acid and still get gout. You can have high uric acid blood level and never get gout. Half the cases of gout occur with low uric acid, the other half with high uric acid.
This idea that meat is somehow involved in disease must stop. It makes no sense that for over 2 million years meat was our staple food therefore kept us in good health, yet in the last 30 years meat has become the death of us. The half-baked hypotheses about the causes of gout tell me the experts don't really know, so they're not really experts.
Yoni gets top marks for his reply
Soo.. to say this is a high protein diet one have to reject all the goverment and all nutrient knowledge about essentiall amino acids!
Its a high fat diet.. IE, a ketogenic diet!
You know, even vegans have there need of essential aminoacids, its the same for us.. the differens is they take it from vegetable sources.. we eat meat/fish/egg/poultry/dairys!
Protein is not that good as fuel.. its more a boulding stone in our bodys!
Generally, rabbit food is not low carbs.
Rabbit as a food is.
The key is to eat plenty of fat, no carbs and not seek high protein foods. If you eat the protein that naturally occurs in meat with fat, you'll probably get enough but not too much.
Like just about everyone else on here, LCHF has been a revelation to me. I was a massive fruit eater - who suffered with very bad arthritis (I had a hip replacement by the time I was 45). I am probably 20lb overweight, not exercising much, and was eating a 'healthy' diet of fruit for breakfast, sandwich for lunch and a paleo dinner.
I've changed my eating habits to incorporate LCHF for about a month and have lost about 4Kg through water-loss so far, and am feeling energised, happy and very well. However, I have two quick questions, if I may:
1. I do still drink about 3 or 4 glasses (maybe upto 750ml) of very dry white cava most evenings, in a social setting. I recognise that this isn't ideal, and I'm working away from it - in the interim could you let me know what problems it causes to drink very dry wine (with minimal sugar) whilst on the LCHF ? I have noticed that it increases my desire for chocolate after I have had a glass or two - but I can resist those urges !!
2. I have taken Barley Grass as a supplement daily for about 2 years. At the moment, my desire for vegetables and other greens is greatly diminished. Is it ok for me to continue to take Barley Grass - and/or will my desire for non animal fat based foods return?
Thanks - and thanks to all the commenters on here too - it's been a life changing event for me to find an eating regime that I can adopt long term that is healthy, balanced - and makes me feel so well. I love it - and I'm losing weight - what's not to like ;)
That about wine and such a thing is more about if one can handel it.. nothing perticuly for a LCHF living!
Mayby if one cut out everything thats not real food one can lose a pound or soo.. thats what its all about.. but one have a life to live altso.
Couldnt be more then fibers and water in Barley grass??
I was having a non-citric fruit smoothie every morning which I suspect was creating havoc with my insulin production and was keeping me chubby ;( I'm happy with the ongoing weightloss: all in good time - and the change in eating habits is making me feel very well. I'm only eating when hungry - and mostly having animal fat products.
I'm still having about 50-100gms of carbs from rice or bread, fried in fat I make from making beef stock dripping as well as loads of eggs, cheese, cream products. I was panicking about my cholesterol level, as it was 'high' last year - and I'm due a check in May - however, I have watched a video today:
that continues to add fuel to my fire that the things I am doing to change my life are going in the right direction. I will, however, be booking a 'particle' blood test to check my cholesterol again against my new understanding.
Your website and the philosophy you have shared is inspiriational ! I'm very excited to be on this journey and will report back in a few months !
Thanks loads, it's been very liberating so far ;)
Its more about if you want to get in extra high ketosis or similar that one need to be an ascetic one!
And you know.. the french do eat a lot of saturated fat and drink wine.. they dont get that much hart attacks!
Soo.. mayby you could call it a mediteranian diet.. french style?
Its always a good idea to check ones healt markers.. and there are a few that not tollerate high fat altso.. but they are rare.. and they supose to know about this alredy.. becuse one or both of there parents do have that condition too.
I do lots of sport and was wondering is there another way to gain muslce mass and weight.
I simply have a LCHF diet for 5-7 days then 1-2 days of LFHC to gain wieght.
is there any other way on protein and fat to put on weight.
I'm no expert but I think I can give you a few ideas. Gary Taubes wrote a book Good Calories Bad Calories. In that book, he makes the argument that fat tissue is regulated by hormones. So, if that's true, then what regulates _muscle_ tissue? Once you figure that out, you'll be able to design a proper muscle-building program.
I mean, if I wanted to design a proper _fat_ building program (you know: grow fatter!), I'd start by eating more carbs. :)
It's not that simple. Insulin is the hormone that regulates fat storage, and that's an entirely different process from building muscle. I know of two books that are dedicated to this topic: "The Smarter Science of Slim" by Jonathan Bailor and "The Art and Science of Low Carb Performance" by Phinney and Voleck.
I also recommend Taubes "Good Calories Bad Calories" but I prefer his newer book "Why we get Fat"
All are on Amazon, bug GCBC may be available only as a used book.
I asked "what regulates muscle tissue", just as Taubes asked "what regulates fat tissue". That's where we start with building muscle. It's that simple. Consider the question Jack asked "is there any other way on protein and fat to put on weight". It's the wrong question because it implies that "protein and fat" is the cause, and "put on weight" is the effect. But my question "what regulates muscle tissue" does not assume an already established cause-and-effect. It _asks_ what the cause and effect is.
Do you believe the bodybuilding world knows how it works? On one side, you got the regular Joes who are told to eat more to grow, eat less to cut, and lift weights in a million different ways. On the other side, you got pro bodybuilders who inject T/GH/IN/IGF/MGF/etc all the while telling the world they grow big by lifting heavy. Truth is pros grow big because of hormones, and they can lift heavy because they're big. Fact: Growth hormone causes muscle growth all on its own without a single weight lifted. It does this through various ways, some of which are growth factors called myostatin and follistatin. Breeding manipulations of genetic traits directly related to those two growth factors in beef produced the Belgian Blue, which has about double the muscle mass, i.e. double the meat.
Ask the right questions. Get the right answers. Don't assume anything. It's that simple.
My concern has been ateroesclerosis if a high fat diet does not cause this then what does?
Why are so many people are having bypasses?
This is my concern that is holding me back I am not saying that any of this is wrong I just need more convincing before I start a LC Diet that's all.
The moste others that have Aterosklerosis problem becuse of Metabolic syndrome.. I.E.. its about glucose metabolism!
"Methods and Results— To represent the progressive stages in the natural history of type 2 diabetes mellitus, we stratified 134 individuals (age 45±12 years) into 1 of 4 groups: (1) lean normoglycemic (lean), (2) overweight and obese normoglycemic (obese), (3) impaired glucose tolerance, and (4) type 2 diabetes mellitus. Localized 1H magnetic resonance spectroscopy and cardiac magnetic resonance imaging were used to quantify myocardial triglyceride content and left ventricular function, respectively. Compared with lean subjects, myocardial triglyceride content was 2.3-fold higher in those with impaired glucose tolerance and 2.1-fold higher in those with type 2 diabetes mellitus (P<0.05). Left ventricular ejection fraction was normal and comparable across all groups.
Conclusions— In humans, impaired glucose tolerance is accompanied by cardiac steatosis, which precedes the onset of type 2 diabetes mellitus and left ventricular systolic dysfunction. Thus, lipid overstorage in human cardiac myocytes is an early manifestation in the pathogenesis of type 2 diabetes mellitus and is evident in the absence of heart failure."
That's the best option for most people.
>>My concern has been ateroesclerosis if a high fat diet does not cause this then what does?
Carbs, mostly. The major risk factors for CVD are low HDL; high TG; high small dense LDL particles; high blood pressure.
All of those improve dramatically for most people on a LCHF diet.
>>Why are so many people are having bypasses?
Because most people eat a high carb diet that makes everyone of those risk factors worse.
>>This is my concern that is holding me back I am not saying that any of this is wrong I just need more convincing before I start a LC Diet that's all.
Check out the studies on the web site, specifically the very first one and the random controlled trials. Look at the impact of diet on the risk factors for CVD.
Cellulite is just fat accumulated in specific areas.
There are no huge differences between LCHF and Atkins. If you got bored with it and did not follow it, you should not be surprised it did not reduce your adipose tissue.
Unfortunately we don't get to decide where we lose the fat. Also, whatever fat cells you have on you are part of your body forever! When you lose weight, the fat cells lose the fat that they contain, but they remain on you nonetheless.
Fat is fat, cellulite is just localized fat. I lost fat by sticking to my low carb diet. It's very slow. I don't think it's really worth trying unless you are dedicated to do whatever it takes to reach your goal, but that's just me.
But low carb absolutely worked to decrease the fat I have on me.
There were no clear effects of dietary fat changes on total mortality or cardiovascular mortality…
Hooper L, et al. Reduced or modified dietary fat for preventing cardiovascular disease. Cochrane Database Syst Rev. 2011 Jul 6;(7):CD002137.
But the first line of the results says:
This updated review suggested that reducing saturated fat by reducing and/or modifying dietary fat reduced the risk of cardiovascular events by 14%
This seems to be saying the opposite. Am I missing something?
And then.. whats the higher risk.. probably biomarkers as cholesterol and such a thing?
Soo.. is those biomarkers dangerus at all??
I think there is a lot of science supporting LCHF for the average person but what about people with Familial Hypercholesteremia (specifically the heterozygous sort)? As this is a liver gene defect which creates abnormally high cholesterol in it's sufferers, do you still recommend LCHF to these patients as well? With FH, modifying the diet has a small effect but not enough and nearly all sufferers of this genetic disease must take statins to bring the cholesterol down to safer levels.
I would be nervous to suggest to someone with FH to eat steak with Bernais sauce every day as well as egg yolks for breakfast every morning with butter. What are you thoughts Doc?
And I dont think there is a good idea for those how have a real FH to rely on a high fat diet.. at least not without cheking there lipids and how its progress!
You know.. its a lot about those with FH and extrapolation from those that give us the fear for fat.. but thats only a misconception.. its the wrong conclusion!
And now the moste problem is the metabolic syndrome.. how have a strong link to glucose metabolism.
Soo.. what its all about.. its about to eat real healty food.. and avoid anyting that is unhealty or that you have a genetic dysfunction to metabolise.
If I selectively read the article I would see your "There were no clear effects of dietary fat changes on total mortality or cardiovascular mortality" HOWEVER Science is not about selecting lines from an article to suit you and misleading people to believe the opposite of what is suggested by the artlcle.
If I were to chose a line I would chose it from the conclusion: "Lifestyle advice to all those at risk of cardiovascular disease and to lower risk population groups, should continue to include permanent reduction of dietary saturated fat and partial replacement by unsaturates."
Also note from the results section: "This updated review suggested that reducing saturated fat by reducing and/or modifying dietary fat reduced the risk of cardiovascular events by 14%"
Your post implies the following assumption: If it's true for the group, then it must also be true for individuals in that group.
Since we're talking about studies, then the equivalent is: If it's true for a group of studies, then it must also be true for individual studies in that group.
This is just an assumption, which means we must check the individual studies to see if our assumption is correct. When we start with the Cochrane study, then check individual studies - as those in the blog post above - we find our assumption is not correct. So what's the problem?
Either our selection of individual studies is biased, or the group of studies is biased. The answer is in the "Selection Criteria" of the Cochrane review: "2) intention to reduce or modify fat or cholesterol intake (excluding exclusively omega-3 fat interventions)". This is "intention to treat".
In scientific studies, the term "intention to treat" means there's no data, but they still assumed there was, so they estimated whatever data was missing, and included this estimation in the results. In other words, they made it up. You could say it's a valid way to find results. I don't. I prefer to consider only hard data. So I ignore any study/review which includes intention-to-treat as a selection criteria or protocol. Unfortunately, this means I should ignore the Cochrane review. And I do ignore it.
In fact, I should ignore the Cochrane review because one of the parameters which justifies intention-to-treat is lack of compliance, and compliance is one the most significant factor for success with dietary intervention. In other words, a diet works as long as we actually do it. In the A-TO-Z study for example, we see that the Atkins group was the most compliant, and also showed the best results. Conversely, success/failure is also a significant factor for compliance, which suggests that compliance was higher with Atkins because it was more successful.
They didnt find any clear effects from reducing fat.. that says me a lot more then there own conclusions.. they couldnt fins anything in the data.. but draw some off topic conclusions anyway!
>>This updated review suggested that reducing saturated fat by reducing and/or modifying dietary fat reduced the risk of cardiovascular events by 14%
>This seems to be saying the opposite. Am I missing something?
Two different measures: Risk for cardiac events and mortality. Reducing saturated fat did not reduce mortality.
As for the risk for cardiac events, it's important to note this: "Subgrouping suggested that this reduction in cardiovascular events was seen in studies of fat modification (not reduction - which related directly to the degree of effect on serum total and LDL cholesterol and triglycerides"
What this suggests is that the risks for caridac events is directly related to LDL and triglycerides. As the bulk of the studies on this page show, a LCHF diet improves blood profile, lowering triglycerides, lowering small LDL and increasing HDL.
It seems clear that reducing saturated fat, while not changing carbohydrate intake does not reduce mortality.
>>>Science is not about selecting lines from an article to suit you and misleading people to believe the opposite of what is suggested by the artlcle.
>>>If I were to chose a line I would chose it from the conclusion: "Lifestyle advice to all those at risk of cardiovascular disease and to lower risk population groups, should continue to include permanent reduction of dietary saturated fat and partial replacement by unsaturates."
But that's not science. That's not data and that's not results. That is simply the opinion of the author.
One of the key arguments made by LCHF diet proponents is that there is a bias in medical and research communities against fat and saturated fat (and in favor of carbs) that is not supported by the evidence. The researchers' conclusions, especially in light of the weak correlations, are perfectly consistent with the suggestion of an unscientific bias.
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