Diet and Skin Health- Raw? Vegetarian? Paleo?
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free skin care · Sun Apr 15, 2012 9:58 am

And if I might add, I think stress reduction and positive attitude are absolutely essential for a fulfilling AND long life and I suspect they are every bit as important as diet. In fact, I saw a study this year coming out of South America (Brazil?) showing that mood had a stronger effect on the immune system than anything else! The results were really impressive. If I find that study, I'll post it here.

free skin care · Sun Apr 15, 2012 4:38 pm

cm5597 wrote:

fitgineer wrote:

Please remember that you are the one that attacked my posts rather aggressively, which I do not appreciate and have been deeply offended by. It's one thing to debate in a mature manner, bringing evidence and stating that you disagree, and another to call someone out the way you did. We are all entitled to our own opinions, and I never quoted you when I first posted on this forum; you pretty much call me a fool for adopting my current diet; just because it doesn't work for you, it doesn't mean it won't work for me; ...

Fitgineer,

I'm deeply sorry my posts had that effect; that was not my intent at all! You are not a fool and no one should be made to feel that way. I sincerely apologize for unintentionally making you feel that way.

I don't doubt and am sincerely glad that whatever you are doing now is much better than whatever you were doing earlier...there are so many variables, so many ways to execute any diet it can complicated to figure out what working and what's not, so kudos in making such great improvements Smile

But I didn't attack your opinion nor your experiences nor did I challenge the benefits you experienced from the changes you made.

I only challenged the points that you said as FACTS--that low fat diets lead to increased risk of diabetes and AGEs. These are factual statements--ones that can be verified or refuted--and you made factual statements that were incorrect. And I feel that we have an obligation to check that these are right when we discuss them in public forums, just as journalists have the same obligation when they write articles for the public. Perhaps I overreacted but I was bothered by what I perceived as a lightness or lack of fulfilling a fundamental obligation in stating serious matters of facts that were actually incorrect and had not been properly researched. As a result, I honestly thought that I was debating these points with you and elevating the calibre of the discussion into being more mature and thorough by explaining in detail why I disagreed, sharing scientific articles with you, and asking you to share scientific articles to support your contention. I'm sorry if you felt otherwise.

Like you, I agree that we should also have the freedom and space to share OPINIONS and EXPERIENCES. And like you, there are some things I do that are not mainstream. However, I'm very careful about the distinction between opinion/experience and facts. For example, I think eating tons of raw foods is fantastic and I think it's one of the best things I've ever done and I'm happy to share my experiences. But you'll never see me make any claims about diabetes risk or disease prevention as there is (virtually) no supporting evidence yet....even though I strongly suspect that it is highly beneficial.

Anyhow, I'm sure we just had a misunderstanding. Unfortunately, I know once a great while these crop up and disagreements happen all the time over EDS. If you haven't yet, many of us learn to develop a thick skin and realize that people are not challenging you as a person in particular but just the merit of something particular that was said. You and the experiences you've had are welcome here just as much as anyone else (me or anyone else), and I would hate for this to sour your experience or prevent you from sharing or having a fantastic experience at EDS. So I'm sincerely, sincerely sorry for having upset you and not coming across better in my posts! Smile

Please PM me if there's anything I can do to better rectify the situation or to help either now or in the future. Smile

I'm so sorry!

I simply did not expect someone to be so aggressive on this forum. But I understand where you are coming from and agree that I should have expressed myself differently. You've definitely taught me a lesson, next time I post something on EDS that I truly believe in, I will add the disclaimer that is only my personal opinion and not that of a subject matter expert. Smile

Hopefully that will not trigger any further attacks from anyone.

free skin care · Mon Apr 16, 2012 12:46 am

For the record, I don't believe that CM was rude or disrespectful in any way. She simply stated her point of view and supported it with links to clinical studies. CM has always contributed a very well informed and researched opinion with regard to many topics. Like myself, I believe it concerns her when she reads information which is blatantly incorrect.

It has to be realised that we are communicating in the written word - and that can sometimes come across in a dry manner - but that doesn't mean that things are stated with any ill intent or disrespect.

free skin care · Mon Apr 16, 2012 10:39 am

Interesting study on PubMed:

Modulation of oxidative stress and mitochondrial function by the ketogenic diet.
Milder J, Patel M.
SourceDepartment of Pharmaceutical Sciences, University of Colorado Denver School of Pharmacy, Aurora, CO 80045, USA.

Abstract
The ketogenic diet (KD) is a high-fat, low carbohydrate diet that is used as a therapy for intractable epilepsy. However, the mechanism(s) by which the KD achieves neuroprotection and/or seizure control are not yet known. The broad efficacy of the KD in diverse epilepsies coupled with its profound influence on metabolism suggests that mitochondrial functions may be critical in its mechanism(s) of seizure control. Mitochondria subserve important cellular functions that include the production of cellular ATP, control of apoptosis, maintenance of calcium homeostasis and the production and elimination of reactive oxygen species (ROS). This review will focus on recent literature reporting the regulation of mitochondrial functions and redox signaling by the KD. The review highlights a potential mechanism of the KD involving the production of low levels of redox signaling molecules such as H(2)O(2) and electrophiles e.g. 4-hydroxynonenal (4-HNE), which in turn activate adaptive pathways such as the protective transcription factor, NF E2-related factor 2 (Nrf2). This can ultimately result in increased production of antioxidants (e.g. GSH) and detoxification enzymes which may be critical in mediating the protective effects of the KD.

Obviously the fat intake would be from healthy fats. I know this article refers to epileptic seisures controlled through KD therapy (same thing they do for migraines), but if a ketogenic diet can result in increased production of antioxidants and detox enzymes, doesn't this mean it would also benefit the skin? Doesn't it mean that glycation is reduced?
And why would they push KD therapy if it leads to degenerative diseases?

Here's a study that might help answer that question:

Low carbohydrate ketogenic diet prevents the induction of diabetes using streptozotocin in rats.
Al-Khalifa A, Mathew TC, Al-Zaid NS, Mathew E, Dashti H.
SourceDepartment of Anatomy, Faculty of Medicine, Health Sciences Center, Kuwait University, Kuwait.

Abstract
Diabetes continues to be an overwhelmingly prevalent endocrine disorder that leads to several micro- and macrocomplications. It has been widely accepted that changes in dietary habits could induce or prevent the onset of diabetes. It is shown that low carbohydrate ketogenic diet (LCKD) is effective in the amelioration of many of the deleterious consequences of diabetes. However, its role in preventing the onset of diabetes is not understood. Therefore, this study is focused on the effect of LCKD in preventing the induction of diabetes using streptozotocin (STZ) in rats by biochemical and histological methods. Forty-two Wistar rats weighing 150-250 g were used in this study. The animals were divided into three groups: normal diet (ND), low carbohydrate ketogenic diet (LCKD), and high carbohydrate diet (HCD). Specific diets ad libitum were given to each group of animals for a period of 8 weeks. Each group was further subdivided into normal control, sham control and diabetic groups. Animals in the diabetic group were given a single intraperitoneal injection of STZ (55 mg/kg). All the animals were sacrificed 4 weeks after the injection of STZ. Daily measurements of food and water intake as well as weekly measurement of body weight were taken during the whole 12 weeks of the experiment. After injecting with STZ, the blood glucose level of all the groups increased significantly except for the group fed on LCKD (p value<0.01). Also, food intake, water intake and urine output were significantly increased in all groups except for the LCKD group (p value<0.01). There was also a significant decrease in the weight gain of the animals that were fed on a LCKD as compared to other groups (p value<0.05). Although, substantial decrease in the number of Î² cells was noticed in diabetic rats, there were no change in the number of Î² cells in the LCKD treated diabetic animals as compared to LCKD control group. The results presented in this study, therefore, suggests that LCKD prevents the development of diabetes using streptozotocin in rats.

I will let you draw your own conclusions. What I have posted above is science. Of course, you can say the studies above are biased, the control groups are chosen to prove their hypothesis, they use additional substances in combination with KD... That's usually the case with many studies. I don't think one can start eating bacon and cheese only every day and stay healthy, but if KD therapy is supervised by a specialist, it might be a good solution for some people.

free skin care · Mon Apr 16, 2012 10:49 am

Keliu wrote:

For the record, I don't believe that CM was rude or disrespectful in any way. She simply stated her point of view and supported it with links to clinical studies. CM has always contributed a very well informed and researched opinion with regard to many topics. Like myself, I believe it concerns her when she reads information which is blatantly incorrect.

It has to be realised that we are communicating in the written word - and that can sometimes come across in a dry manner - but that doesn't mean that things are stated with any ill intent or disrespect.

Thanks Keliu for clarifying. I tried to post scientific evidence in my previous post.

free skin care · Mon Apr 16, 2012 11:01 am

fitgineer wrote:

Interesting study on PubMed:

Modulation of oxidative stress and mitochondrial function by the ketogenic diet.
Milder J, Patel M.
SourceDepartment of Pharmaceutical Sciences, University of Colorado Denver School of Pharmacy, Aurora, CO 80045, USA.

Abstract
The ketogenic diet (KD) is a high-fat, low carbohydrate diet that is used as a therapy for intractable epilepsy. However, the mechanism(s) by which the KD achieves neuroprotection and/or seizure control are not yet known. The broad efficacy of the KD in diverse epilepsies coupled with its profound influence on metabolism suggests that mitochondrial functions may be critical in its mechanism(s) of seizure control. Mitochondria subserve important cellular functions that include the production of cellular ATP, control of apoptosis, maintenance of calcium homeostasis and the production and elimination of reactive oxygen species (ROS). This review will focus on recent literature reporting the regulation of mitochondrial functions and redox signaling by the KD. The review highlights a potential mechanism of the KD involving the production of low levels of redox signaling molecules such as H(2)O(2) and electrophiles e.g. 4-hydroxynonenal (4-HNE), which in turn activate adaptive pathways such as the protective transcription factor, NF E2-related factor 2 (Nrf2). This can ultimately result in increased production of antioxidants (e.g. GSH) and detoxification enzymes which may be critical in mediating the protective effects of the KD.

Obviously the fat intake would be from healthy fats. I know this article refers to epileptic seisures controlled through KD therapy (same thing they do for migraines), but if a ketogenic diet can result in increased production of antioxidants and detox enzymes, doesn't this mean it would also benefit the skin? Doesn't it mean that glycation is reduced?
And why would they push KD therapy if it leads to degenerative diseases?

Here's a study that might help answer that question:

Low carbohydrate ketogenic diet prevents the induction of diabetes using streptozotocin in rats.
Al-Khalifa A, Mathew TC, Al-Zaid NS, Mathew E, Dashti H.
SourceDepartment of Anatomy, Faculty of Medicine, Health Sciences Center, Kuwait University, Kuwait.

Abstract
Diabetes continues to be an overwhelmingly prevalent endocrine disorder that leads to several micro- and macrocomplications. It has been widely accepted that changes in dietary habits could induce or prevent the onset of diabetes. It is shown that low carbohydrate ketogenic diet (LCKD) is effective in the amelioration of many of the deleterious consequences of diabetes. However, its role in preventing the onset of diabetes is not understood. Therefore, this study is focused on the effect of LCKD in preventing the induction of diabetes using streptozotocin (STZ) in rats by biochemical and histological methods. Forty-two Wistar rats weighing 150-250 g were used in this study. The animals were divided into three groups: normal diet (ND), low carbohydrate ketogenic diet (LCKD), and high carbohydrate diet (HCD). Specific diets ad libitum were given to each group of animals for a period of 8 weeks. Each group was further subdivided into normal control, sham control and diabetic groups. Animals in the diabetic group were given a single intraperitoneal injection of STZ (55 mg/kg). All the animals were sacrificed 4 weeks after the injection of STZ. Daily measurements of food and water intake as well as weekly measurement of body weight were taken during the whole 12 weeks of the experiment. After injecting with STZ, the blood glucose level of all the groups increased significantly except for the group fed on LCKD (p value<0.01). Also, food intake, water intake and urine output were significantly increased in all groups except for the LCKD group (p value<0.01). There was also a significant decrease in the weight gain of the animals that were fed on a LCKD as compared to other groups (p value<0.05). Although, substantial decrease in the number of Î² cells was noticed in diabetic rats, there were no change in the number of Î² cells in the LCKD treated diabetic animals as compared to LCKD control group. The results presented in this study, therefore, suggests that LCKD prevents the development of diabetes using streptozotocin in rats.

I will let you draw your own conclusions. What I have posted above is science. Of course, you can say the studies above are biased, the control groups are chosen to prove their hypothesis, they use additional substances in combination with KD... That's usually the case with many studies. I don't think one can start eating bacon and cheese only every day and stay healthy, but if KD therapy is supervised by a specialist, it might be a good solution for some people.

I would like to show how research seems to be all over the place, and why I go back to my IV comment before. The study below shows a side of KD that is not necessarily a good one:

A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain.
Jornayvaz FR, Jurczak MJ, Lee HY, Birkenfeld AL, Frederick DW, Zhang D, Zhang XM, Samuel VT, Shulman GI.
SourceDepts. of Internal Medicine, Yale Univ. School of Medicine, New Haven, CT 06536, USA.

Abstract
Low-carbohydrate, high-fat ketogenic diets (KD) have been suggested to be more effective in promoting weight loss than conventional caloric restriction, whereas their effect on hepatic glucose and lipid metabolism and the mechanisms by which they may promote weight loss remain controversial. The aim of this study was to explore the role of KD on liver and muscle insulin sensitivity, hepatic lipid metabolism, energy expenditure, and food intake. Using hyperinsulinemic-euglycemic clamps, we studied insulin action in mice fed a KD or regular chow (RC). Body composition was assessed by ï¿½H magnetic resonance spectroscopy. Despite being 15% lighter (P < 0.001) than RC-fed mice because of a 17% increase in energy expenditure (P < 0.001), KD-fed mice manifested severe hepatic insulin resistance, as reflected by decreased suppression (0% vs. 100% in RC-fed mice, P < 0.01) of endogenous glucose production during the clamp. Hepatic insulin resistance could be attributed to a 350% increase in hepatic diacylglycerol content (P < 0.001), resulting in increased activation of PKCÎµ (P < 0.05) and decreased insulin receptor substrate-2 tyrosine phosphorylation (P < 0.01). Food intake was 56% (P < 0.001) lower in KD-fed mice, despite similar caloric intake, and could partly be attributed to a more than threefold increase (P < 0.05) in plasma N-acylphosphatidylethanolamine concentrations. In conclusion, despite preventing weight gain in mice, KD induces hepatic insulin resistance secondary to increased hepatic diacylglycerol content. Given the key role of nonalcoholic fatty liver disease in the development of type 2 diabetes and the widespread use of KD for the treatment of obesity, these results may have potentially important clinical implications.

So, what do you make of it? KD increases antioxidants, detox enzymes, prevents diabetes in conjunction with another substance, but increases hepatic insulin resistance (which can lead to diabetes?)... What is then KD's net effect on glycation? Is there a way to find the perfect balance in one's diet?

free skin care · Mon Apr 16, 2012 11:13 am

fitgineer wrote:

Interesting study on PubMed:

Modulation of oxidative stress and mitochondrial function by the ketogenic diet.
Milder J, Patel M.
SourceDepartment of Pharmaceutical Sciences, University of Colorado Denver School of Pharmacy, Aurora, CO 80045, USA.

Abstract
The ketogenic diet (KD) is a high-fat, low carbohydrate diet that is used as a therapy for intractable epilepsy. However, the mechanism(s) by which the KD achieves neuroprotection and/or seizure control are not yet known. The broad efficacy of the KD in diverse epilepsies coupled with its profound influence on metabolism suggests that mitochondrial functions may be critical in its mechanism(s) of seizure control. Mitochondria subserve important cellular functions that include the production of cellular ATP, control of apoptosis, maintenance of calcium homeostasis and the production and elimination of reactive oxygen species (ROS). This review will focus on recent literature reporting the regulation of mitochondrial functions and redox signaling by the KD. The review highlights a potential mechanism of the KD involving the production of low levels of redox signaling molecules such as H(2)O(2) and electrophiles e.g. 4-hydroxynonenal (4-HNE), which in turn activate adaptive pathways such as the protective transcription factor, NF E2-related factor 2 (Nrf2). This can ultimately result in increased production of antioxidants (e.g. GSH) and detoxification enzymes which may be critical in mediating the protective effects of the KD.

Obviously the fat intake would be from healthy fats. I know this article refers to epileptic seisures controlled through KD therapy (same thing they do for migraines), but if a ketogenic diet can result in increased production of antioxidants and detox enzymes, doesn't this mean it would also benefit the skin? Doesn't it mean that glycation is reduced?
And why would they push KD therapy if it leads to degenerative diseases?

Here's a study that might help answer that question:

Low carbohydrate ketogenic diet prevents the induction of diabetes using streptozotocin in rats.
Al-Khalifa A, Mathew TC, Al-Zaid NS, Mathew E, Dashti H.
SourceDepartment of Anatomy, Faculty of Medicine, Health Sciences Center, Kuwait University, Kuwait.

Abstract
Diabetes continues to be an overwhelmingly prevalent endocrine disorder that leads to several micro- and macrocomplications. It has been widely accepted that changes in dietary habits could induce or prevent the onset of diabetes. It is shown that low carbohydrate ketogenic diet (LCKD) is effective in the amelioration of many of the deleterious consequences of diabetes. However, its role in preventing the onset of diabetes is not understood. Therefore, this study is focused on the effect of LCKD in preventing the induction of diabetes using streptozotocin (STZ) in rats by biochemical and histological methods. Forty-two Wistar rats weighing 150-250 g were used in this study. The animals were divided into three groups: normal diet (ND), low carbohydrate ketogenic diet (LCKD), and high carbohydrate diet (HCD). Specific diets ad libitum were given to each group of animals for a period of 8 weeks. Each group was further subdivided into normal control, sham control and diabetic groups. Animals in the diabetic group were given a single intraperitoneal injection of STZ (55 mg/kg). All the animals were sacrificed 4 weeks after the injection of STZ. Daily measurements of food and water intake as well as weekly measurement of body weight were taken during the whole 12 weeks of the experiment. After injecting with STZ, the blood glucose level of all the groups increased significantly except for the group fed on LCKD (p value<0.01). Also, food intake, water intake and urine output were significantly increased in all groups except for the LCKD group (p value<0.01). There was also a significant decrease in the weight gain of the animals that were fed on a LCKD as compared to other groups (p value<0.05). Although, substantial decrease in the number of Î² cells was noticed in diabetic rats, there were no change in the number of Î² cells in the LCKD treated diabetic animals as compared to LCKD control group. The results presented in this study, therefore, suggests that LCKD prevents the development of diabetes using streptozotocin in rats.

I will let you draw your own conclusions. What I have posted above is science. Of course, you can say the studies above are biased, the control groups are chosen to prove their hypothesis, they use additional substances in combination with KD... That's usually the case with many studies. I don't think one can start eating bacon and cheese only every day and stay healthy, but if KD therapy is supervised by a specialist, it might be a good solution for some people.

I would like to show how research seems to be all over the place, and why I go back to my IV comment before. The study below shows a side of KD that is not necessarily a good one:

A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain.
Jornayvaz FR, Jurczak MJ, Lee HY, Birkenfeld AL, Frederick DW, Zhang D, Zhang XM, Samuel VT, Shulman GI.
SourceDepts. of Internal Medicine, Yale Univ. School of Medicine, New Haven, CT 06536, USA.

Abstract
Low-carbohydrate, high-fat ketogenic diets (KD) have been suggested to be more effective in promoting weight loss than conventional caloric restriction, whereas their effect on hepatic glucose and lipid metabolism and the mechanisms by which they may promote weight loss remain controversial. The aim of this study was to explore the role of KD on liver and muscle insulin sensitivity, hepatic lipid metabolism, energy expenditure, and food intake. Using hyperinsulinemic-euglycemic clamps, we studied insulin action in mice fed a KD or regular chow (RC). Body composition was assessed by ï¿½H magnetic resonance spectroscopy. Despite being 15% lighter (P < 0.001) than RC-fed mice because of a 17% increase in energy expenditure (P < 0.001), KD-fed mice manifested severe hepatic insulin resistance, as reflected by decreased suppression (0% vs. 100% in RC-fed mice, P < 0.01) of endogenous glucose production during the clamp. Hepatic insulin resistance could be attributed to a 350% increase in hepatic diacylglycerol content (P < 0.001), resulting in increased activation of PKCÎµ (P < 0.05) and decreased insulin receptor substrate-2 tyrosine phosphorylation (P < 0.01). Food intake was 56% (P < 0.001) lower in KD-fed mice, despite similar caloric intake, and could partly be attributed to a more than threefold increase (P < 0.05) in plasma N-acylphosphatidylethanolamine concentrations. In conclusion, despite preventing weight gain in mice, KD induces hepatic insulin resistance secondary to increased hepatic diacylglycerol content. Given the key role of nonalcoholic fatty liver disease in the development of type 2 diabetes and the widespread use of KD for the treatment of obesity, these results may have potentially important clinical implications.

So, what do you make of it? KD increases antioxidants, detox enzymes, prevents diabetes in conjunction with another substance, but increases hepatic insulin resistance (which can lead to diabetes?)... What is then KD's net effect on glycation? Is there a way to find the perfect balance in one's diet?

Yet another paper... I think it points to that balance/moderation we should achieve:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3243104/

"There is evidence that the brain favors consumption of carbohydrates (CHO) rather than fats, this preference resulting in glycolysis-based energy metabolism domination. This metabolic mode, typical for consumers of the ï¿½Western dietï¿½ (Cordain et al., 2005; Seneff et al., 2011), is characterized by over-generation of reactive oxygen species and advanced glycation products both of which are implicated in many of the neurodegenerative diseases (Tessier, 2010; Vicente Miranda and Outeiro, 2010; Auburger and Kurz, 2011). However, it is not CHO but fat that is often held responsible for metabolic pathologies. This paper, based on analysis of experimental data, offers an opinion that the obesogenic and neurodegenerative effects of dietary fat in the high-fat diets (HFD) cannot be separated from the effects of the CHO compound in them."

I think it's key that the author points out that carbohydrates and fats are interlinked and their effects cannot be separated when ingested together. Or am I reading this wrong?

From the article's conclusion:
"To maximize energy stores, energy intake relies on CHO-driven behaviors to allow the environmental ï¿½push.ï¿½ Therefore: (1) dietary fat is not to blame for the diet-induced obesity; it is CHO that is not limited enough in HFD; (2) KR [ketogenic ratio] may be an element of common language in experiments with different methodological approaches."

Of course, this just another opinion in the scientific world.

free skin care · Mon Apr 16, 2012 4:06 pm

fitgineer wrote:

Is there a way to find the perfect balance in one's diet?

YES!! Eat ALL food groups in moderation and try to focus on whole foods instead of processed ones.

free skin care · Mon Apr 16, 2012 5:25 pm

Keliu wrote:

fitgineer wrote:

Is there a way to find the perfect balance in one's diet?

YES!! Eat ALL food groups in moderation and try to focus on whole foods instead of processed ones.

Exactly, Bravo yet again Keliu! Very Happy

When did eating for sustenance become Rocket Science?
Common sense, moderation, balance.

free skin care · Wed Apr 18, 2012 11:58 am

Keliu wrote:

So far what I've learned from this thread is:

- cooking food is bad
- eating meat is bad
- eating rice, bread and potatoes is bad
- eating fruit is bad
- eating most vegetables is bad
- eating dairy is bad
- eating every day is bad

It's lunch time now - I think I'll just have a glass of water. But hang on, tap water is bad and drinking too much of it can kill you. Looks like I'll have to make it a fast day!

Personally, I think all of you who worry so much about what you eat will die of stress related diseases long before you become old enough to develop diseases from your poor diets.

Explore Paleo, read Mark's Daily Apple. It will begin to make sense to you. You can also explore eating for your genetics, helps sort out some of the fine details of what foods will work for you and which ones won't- also known as metabolic typing and can cost upwards of $250 for a nutritionist to do.
Eating it all in moderation- eh sure, but some foods like dairy and wheat wreak such havoc-- if you are sensitive to them-- it's hardly worth it and not the best advice imo.

free skin care · Wed Apr 18, 2012 7:04 pm

We've been talking about diet and the recommendations of nutritionists, but in these discussions I think some people are missing the main point of food - and that is to provide the body with a variety of nutrients that are essential to its well-being.

All foods contain nutrients in various guises. If you choose not to eat one food group, for example if you choose not to eat animal products for ethical reasons or if you have allergies or food intolerances, then you must try to find the nutrition that is in those foods in others - otherwise you will be depriving your body of essential nutrients. Basically, it's just logic and common sense.

Whilst you might think that your body is perfectly healthy now given the choices you make - it may be a very different scenario down the track. Unhealthy life-style choices will show up after the age of 50 - if you have eaten insufficient amounts of anti-oxidants, or products containing calcium and have eaten too many foods high in animal fats and low in complex carbs - this will all show up in your general health as you age.

Here is a rather good definition of nutrition and an explanation of the different food groups and why we need them:

http://medical-dictionary.thefreedictionary.com/nutrition

free skin care · Thu Apr 19, 2012 6:39 pm

Keliu wrote:

We've been talking about diet and the recommendations of nutritionists, but in these discussions I think some people are missing the main point of food - and that is to provide the body with a variety of nutrients that are essential to its well-being.

All foods contain nutrients in various guises. If you choose not to eat one food group, for example if you choose not to eat animal products for ethical reasons or if you have allergies or food intolerances, then you must try to find the nutrition that is in those foods in others - otherwise you will be depriving your body of essential nutrients. Basically, it's just logic and common sense.

Whilst you might think that your body is perfectly healthy now given the choices you make - it may be a very different scenario down the track. Unhealthy life-style choices will show up after the age of 50 - if you have eaten insufficient amounts of anti-oxidants, or products containing calcium and have eaten too many foods high in animal fats and low in complex carbs - this will all show up in your general health as you age.

Here is a rather good definition of nutrition and an explanation of the different food groups and why we need them:

http://medical-dictionary.thefreedictionary.com/nutrition

No we don't "need" all food groups to be healthy- that is pure bull. I eat very little dairy and few grains and am better off for doing so.
Again, Mark Sisson gives good advice:
http://www.marksdailyapple.com/how-to-succeed-with-the-primal-blueprint/#axzz1sXZQ5VWS

free skin care · Thu Apr 19, 2012 7:37 pm

gretchen wrote:

No we don't "need" all food groups to be healthy- that is pure bull. I eat very little dairy and few grains and am better off for doing so.

You stated earlier in the thread that you eat a stick of butter in one hit - that is far more dairy than most people consume.

You are free to follow the advice of anyone - but I think it's illogical to simply call the bulk of medical opinion "bull".

free skin care · Fri Apr 20, 2012 6:17 am

Keliu wrote:

gretchen wrote:

No we don't "need" all food groups to be healthy- that is pure bull. I eat very little dairy and few grains and am better off for doing so.

You stated earlier in the thread that you eat a stick of butter in one hit - that is far more dairy than most people consume.

You are free to follow the advice of anyone - but I think it's illogical to simply call the bulk of medical opinion "bull".

Forgive me for agreeing I really hope this will cause the page to change!

BTW Gretchen check your photobucket account, you can RE-SIZE your pictures/graphics so they aren't so Huge.

Thanks Very Happy

free skin care · Fri Apr 20, 2012 10:34 am

I've been reading diet/nutrition and health related books/blogs etc. for what feels like a million years and you know what? I don't jump on bandwagons any more.

Bandwagons are led by booksellers (if you quote me on that, please give me credit lol).....

Every so often, somebody new jumps into the circle, claiming that if you just manipulate your diet according to:

- macronutrient ratios
- calorie levels
- meal timing
- whether the food is raw or cooked
- whether the food is liquid or solid
- whether the foods come from animals or plants
- what kinds of foods you eat
- how you combine those foods
- before/after/during exercise
- if you would just eat coconut oil or chia seeds or...or...
etc. etc. - that will be the magic bullet to lifelong health and happiness and you know what?

...there is no consensus folks! every bandwagon pulls out it own selective scientific studies to prove its points...

At some point you have to use your own common sense...don't rely on the government, don't rely on the food manufacturers or booksellers...rely on yourself. You know what's best for you already.

What's best for me?

A whole foods diet - as unprocessed as I can possibly get it, de-emphasis on grain or starchy, sugary carbs due to family history of diabetes, but just enough very complex carbs to support exercise and endurance... care with animal based foods - where they come from, how they were raised, etc.

What does a meal look like?
- some kind of animal or plant protein with lots of green and or colorful veggies and a bit of healthy oil dressing or grass fed butter - glass of wine (sometimes a big glass!)

Fruit or coffee or bit of dark chocolate for dessert.
Sometimes I just make a protein smoothie with fruit.

On holidays or special occasions, I might have some of what others are having...and that's it - pretty simple.

I usually only eat one meal/day because I think IF is healthy, so easy and saves money.
I drink good coffee and good tea, some kombucha and kefir...

When I want to lose weight, I cut back on the amounts and do without the wine, chocolate and any extra fruit...

I do not support any particular booksellers or bloggers, but do second the rec on Mark Sisson and the guy who writes the Bulletproof Diet (forget his name) You can download, for free - his chart, which I think is a good one...but
I don't think you need to delve deeply into books or blogs to know intuitively what is healthy to eat...

BFG

free skin care · Sat Apr 21, 2012 2:56 pm

Keliu wrote:

gretchen wrote:

No we don't "need" all food groups to be healthy- that is pure bull. I eat very little dairy and few grains and am better off for doing so.

You stated earlier in the thread that you eat a stick of butter in one hit - that is far more dairy than most people consume.

You are free to follow the advice of anyone - but I think it's illogical to simply call the bulk of medical opinion "bull".

I process butter well but not most other dairy- it's a genetic thing.
Butter is actually very good for many blood type Os and contains something called butrayte which helps heal the digestive tract and assists with celiac, something that many Os have. I have also lost body fat since increasing my butter intake- my waistline is down to 23-24 inches, a size 0. I am not remotely starving myself either. :-----)

http://huntgatherlove.com/category/tags/dairy
Another hypothesis is that lack of SCFAs is behind such diseases of civilization. A SCFA called butyrate provides some insight into this. Butyrate is the preferred fuel of the colonic epithelial cells and also plays a major role in the regulation of cell proliferation and differentiation (Wong, de Souza, Kendall, Emam, & D. J. a Jenkins, 2006). Lower than normal levels have been found in patients with several diseases, notably types of colitis and inflammatory bowel disorder. Studies show such diseases can be treated through application of butyrate in the colon. That and the fact that some studies show complete remission through bacteriotherapy transplants point to these diseases being caused by disturbed populations of gut bacteria. Interestingly, these diseases are common in captive populations of apes and unheard of in wild apes (McKenna et al., 2008).

http://wholehealthsource.blogspot.com/2009/12/butyric-acid-ancient-controller-of.html
Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance

Susceptible strains of rodents fed high-fat diets overeat, gain fat and become profoundly insulin resistant. Dr. Jianping Ye's group recently published a paper showing that the harmful metabolic effects of a high-fat diet (lard and soybean oil) on mice can be prevented, and even reversed, using a short-chain saturated fatty acid called butyric acid (hereafter, butyrate). [BUTTER] Here's a graph of the percent body fat over time of the two groups:

The butyrate-fed mice remained lean and avoided metabolic problems. Butyrate increased their energy expenditure by increasing body heat production and modestly increasing physical activity. It also massively increased the function of their mitochondria, the tiny power plants of the cell.

free skin care · Mon Apr 23, 2012 12:18 pm

I was just wondering if anyone has tried benfotiamine (fat soluble B1) to reduce glycation as a result of certain food intake?
I have found studies on it, but in humans, in order to see a significant benefit, it seems they need to take a much higher dose/concentration than what the current supplements provide...
Plus, the study below is on diabetic patients, which doesn't mean that it will work the same on healthy subjects (it goes against the no-antioxidants idea mentioned on this thread earlier...)

Quote:

Oral benfotiamine plus alpha-lipoic acid normalises complication-causing pathways in type 1 diabetes.
Du X, Edelstein D, Brownlee M.
SourceJDRF International Center for Diabetic Complications Research, Albert Einstein College of Medicine, Morris Park Avenue F-531, Bronx, NY 10461, USA.

Abstract
AIMS/HYPOTHESIS: We determined whether fixed doses of benfotiamine in combination with slow-release alpha-lipoic acid normalise markers of reactive oxygen species-induced pathways of complications in humans.

METHODS: Male participants with and without type 1 diabetes were studied in the General Clinical Research Centre of the Albert Einstein College of Medicine. Glycaemic status was assessed by measuring baseline values of three different indicators of hyperglycaemia. Intracellular AGE formation, hexosamine pathway activity and prostacyclin synthase activity were measured initially, and after 2 and 4 weeks of treatment.

RESULTS: In the nine participants with type 1 diabetes, treatment had no effect on any of the three indicators used to assess hyperglycaemia. However, treatment with benfotiamine plus alpha-lipoic acid completely normalised increased AGE formation, reduced increased monocyte hexosamine-modified proteins by 40% and normalised the 70% decrease in prostacyclin synthase activity from 1,709 +/- 586 pg/ml 6-keto-prostaglandin F(1alpha) to 4,696 +/- 533 pg/ml.

CONCLUSIONS/INTERPRETATION: These results show that the previously demonstrated beneficial effects of these agents on complication-causing pathways in rodent models of diabetic complications also occur in humans with type 1 diabetes.

Source: http://www.ncbi.nlm.nih.gov/pubmed/18663426

Quote:

Abstract
BACKGROUND: Complications in diabetes mellitus are partially mediated by enhanced formation of reactive oxygen species. Among the factors involved in reactive oxygen species formation, advanced glycation end products play a key role. Owing to a reduced activity of the enzyme transketolase, which requires diphosphorylated thiamine (vitamin B(1)) as cofactor, an accumulation of those deleterious glucose metabolites especially in diabetic patients can be observed. Benfotiamine, a lipophilic thiamine diphosphate prodrug, prevented early renal and retinal changes in animal studies, and reduced neuropathic pain in clinical studies. Several mechanisms for these activities have been described. We investigated for the first time direct antioxidant abilities of benfotiamine. Additionally, a potential DNA protective effect of benfotiamine was analysed.

METHODS: Oxidative stress was detected by flow cytometry, antioxidative capacity was measured with the ferric reducing ability of plasma (FRAP) assay, two endpoints for genomic damage were assessed: the comet assay and the micronucleus test, and the expression and activity of transketolase was quantified.

RESULTS: Benfotiamine prevented oxidative stress induced by the mutagen 4-nitroquinoline-1-oxide (NQO), the uremic toxin indoxyl sulfate, and the peptide hormone angiotensin II in three different kidney cell lines. Cell-free experiments showed a direct antioxidant effect of benfotiamine, which might account for the protective effect. Oxidative DNA damage, induced by angiotensin II, was completely prevented by benfotiamine. Incubation with benfotiamine increased transketolase expression and activity in the cells.

CONCLUSIONS: Benfotiamine shows a direct antioxidant action. This effect of benfotiamine may be involved in the improvement of diabetic late complications, including peripheral neuropathy.

Source: http://www.ncbi.nlm.nih.gov/pubmed/18384109

Here's another one about benfotiamine increasing glucose oxidation:
http://www.ncbi.nlm.nih.gov/pubmed/21984258

free skin care · Sun Jun 17, 2012 7:45 am

Sorry I've been gone for so long here. Just catching up with posts on this subboard.

My *understanding*, FWIW, since I'm not an expert in this field is that the majority of studies show that high fat diets are the larger culprit for insulin resistance, which is not the same thing as diabetes, but it is a primary cause. Because if your body struggles to transport sugar out of your bloodstream and into your cells (which is what insulin resistance is), then that leaves you vulnerable to high blood sugar.

However, you can reduce blood sugar to a degree through a ketogenic diet, too. Sound paradoxical? It's not entirely. High carb consumption (if not accompanied by fiber, so especially refined sugar) OR a ketogenic diet can prevent spikes in blood sugar, that is, they both slow down how quickly sugar ENTERS the bloodstream. However, it's fats that impair the EXIT (transport) of sugars from the bloodstream into the cells, leading to insulin resistance.

So carbs (unrefined, high fiber) = good for blood sugar exit from the blood stream, but either high carbs (unrefined, high fiber) or high fats = good for slowing down entry into the blood stream. Conversely, refined / high glycemic carbs + high fat meal = recipe for disaster, as you spike your blood sugar and prevent it from naturally lowering by impairing the transport to cells.

I hope this make sense.

Just my interpretation of what I've read...hope this helps! Smile

free skin care · Sun Jun 17, 2012 11:28 am

cm5597 wrote:

Sorry I've been gone for so long here. Just catching up with posts on this subboard.

My *understanding*, FWIW, since I'm not an expert in this field is that the majority of studies show that high fat diets are the larger culprit for insulin resistance, which is not the same thing as diabetes, but it is a primary cause. Because if your body struggles to transport sugar out of your bloodstream and into your cells (which is what insulin resistance is), then that leaves you vulnerable to high blood sugar.

However, you can reduce blood sugar to a degree through a ketogenic diet, too. Sound paradoxical? It's not entirely. High carb consumption (if not accompanied by fiber, so especially refined sugar) OR a ketogenic diet can prevent spikes in blood sugar, that is, they both slow down how quickly sugar ENTERS the bloodstream. However, it's fats that impair the EXIT (transport) of sugars from the bloodstream into the cells, leading to insulin resistance.

So carbs (unrefined, high fiber) = good for blood sugar exit from the blood stream, but either high carbs (unrefined, high fiber) or high fats = good for slowing down entry into the blood stream. Conversely, refined / high glycemic carbs + high fat meal = recipe for disaster, as you spike your blood sugar and prevent it from naturally lowering by impairing the transport to cells.

I hope this make sense.

Just my interpretation of what I've read...hope this helps! Smile

Starches like grains and polyunsaturated fats are the problem; eaten together they create diabetes, metabolic syndrome and are certainly pro aging. Healthy saturated fats like coconut oil are shown to increase the metabolism and are therefore anti aging.

The ketogenic diet is not scientific; we actually need good carbs from sugar and fructose to maintain metabolism:
http://raypeat.com/articles/articles/sugar-issues.shtml
http://raypeat.com/articles/articles/glycemia.shtml

The glycemic is stupid.
Smile

http://raypeat.com/articles/articles/glycemia.shtml

When the idea of "glycemic index" was being popularized by dietitians, it was already known that starch, consisting of chains of glucose molecules, had a much higher index than fructose and sucrose. The more rapid appearance of glucose in the blood stimulates more insulin, and insulin stimulates fat synthesis, when there is more glucose than can be oxidized immediately. If starch or glucose is eaten at the same time as polyunsaturated fats, which inhibit its oxidation, it will produce more fat. Many animal experiments show this, even when they are intending to show the dangers of fructose and sucrose.

Watch:
http://www.youtube.com/watch?v=lzlcFVUa7T8

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