Diet Thread

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CKinnard
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Re: Diet Thread

Postby CKinnard » Sun Oct 21, 2018 6:50 pm

I remember when Pritikin was a rising star. Because I was vegetarian then, I bought one of his books. There was little around with as much science-y stuff in it. I hadn't yet discovered McDougall's books. This was around 1978. A lot of runners were getting into eating mostly vegetarian. Runner's World magazine was a major source of info for runners around the world, had an excellent reputation, and was favorable towards Pritikin. When I look back, I think Nathan was a courageous and honorable man to take the journey he did. But I also think it was incredibly sad that he decided to take his own life due to pain related to leukemia. I am not saying that judgementally, as I think there are levels of pain that would drive all of us to suicide.

I think this is a special legacy (source Wikipedia entry for him)

"In the early to mid 1980s, he began to suffer severe pain and complications related to leukemia. He committed suicide at Albany Medical Center on February 21, 1985.[1][2] An autopsy undertaken after Pritikin's death in 1985 revealed absence of atheroscelerosis with only minor streaking noting that the hearts pumping function was uncompromised. "

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Re: Diet Thread

Postby Nobody » Mon Oct 22, 2018 9:42 am

Hi CK,

Revisiting this from the "YES--Insulin Resistance/Diabetes is CAUSED by Fat Intake" video I posted on 19th Oct.

CKinnard wrote:This lady's skewed perspective is all you have to do is reduce saturated fat, and your insulin resistance will reverse, just like spudfit did. Why? because saturated fat CAUSES insulin resistance! But she overlooks that spudfit was on a big Calorie deficit.

The only point I was trying to make from the rat study at 07:55 was that in rats, saturated, mono and PUFA omegs-6 fats all caused insulin resistance. Many try to pin it primarily on saturated fat. But it appears all fats are problematic as there is little omega-3 fat isolated in our natural environment. Even linseed has enough other fats to be problematic if you one gets too much. Being a rat study, it can only be a pointer as to what would happen in humans. But it could explain why some people who avoid saturated fat may still have insulin resistance.

In the video at 12:20. It was one of spudfit's followers/clients that had diabetes for 20 years and reversed it in a week with a very low fat diet. I went looking for the reference on the SpudFit site, but couldn't find it. I don't know anything about if he was on a net calorie deficit or not. But the potato diet is about 1% of calories from fat. So if all fat is the issue with insulin resistance, then a 1% fat diet should significantly help. I'm trailing a 6 - 8% fat diet for about a month or more to see if my cholesterol profile improves. In theory it should also improve my insulin sensitivity.

CKinnard
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Re: Diet Thread

Postby CKinnard » Mon Oct 22, 2018 9:57 am

Nobody wrote:Hi CK,

Revisiting this from the "YES--Insulin Resistance/Diabetes is CAUSED by Fat Intake" video I posted on 19th Oct.
.


I am happy to explore these topics with you Nobody. I'm not trying to be adversarial.

Re whether Spudfit was on a Calorie deficit, objectively speaking, the only way a deficit can be confirmed is via weight loss.
From https://spudfit.com/f-a-q

__________________________
Have you maintained your weight loss since finishing the Spud Fit Challenge?

Over the month of January, following the completion of my Spud Fit Challenge, I lost another 2kg (4lbs). This took my total weight loss to 55kg (121lbs) and meant I weighed the same as I did when I was 15 years old – 96kg (211lbs)! Since then I’ve stopped weighing myself so I can’t be sure of what I actually weigh, my new clothes still all fit though and I still feel good so I guess my weight is around the same (nearly 15 months later at the time of writing this).

Did this change your food addiction?

In short, yes! In the last 15 months I have not eaten any junk food whatsoever, I didn’t even have cake on my birthday. I don’t have any desire to eat any of the foods that got me into the mess I was in. This is not purely because I ate potatoes for a year though. From the beginning I’ve always said potatoes are great but in the end they are just a vehicle that has allowed me to take a break from food. The Spud Fit Challenge gave me the time and space I needed in order to do some important internal work. I learned many lessons from The Spud Fit Challenge and I continue to put them into practice daily in order to maintain my new, healthy relationship with food.


Will this help my diabetes, blood pressure, arthritis, cholesterol, IBS etc?

Yes I expect that it will. I’ve supervised many people through their own Spud Fit Challenges and seen amazing improvements in all of the above conditions and many more. I am yet to hear from someone who followed the rules properly and didn’t have major improvements in their health. As stated above, you should do this under medical supervision.
______________________________


The issue with reversing diabetes is any Calorie deficit can normalize blood glucose within 2 days. There are many studies from the WFPB and LC camps that don't control for weight loss (or the other factors mentioned in my earlier post) when examining effect on diabetes.

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Re: Diet Thread

Postby Nobody » Mon Oct 22, 2018 10:05 am

CKinnard wrote:I've even seen a lack of objectivity from Michael Greger.

Yes I remember when he quoted a study in relative risk terms and not absolute risk. Popper without naming him, called him out on it in one of her videos. Unfortunately it was one of Greger's videos I posted in this thread IIRC. :oops:

CKinnard wrote:What's apparent to me is nutrition is extremely difficult to stay on top of. One would have to read at least 10 hours most weeks after graduating to do so I think. When you only make money by having clients sitting in front of you, that's a tough gig.

I heard that McDougall used to do this. You'd have to if you were going to write an informative monthly newsletter. Which he retired from after Sept, 2017.
https://www.drmcdougall.com/health/education/newsletter/
Last edited by Nobody on Mon Oct 22, 2018 10:15 am, edited 1 time in total.

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Re: Diet Thread

Postby Nobody » Mon Oct 22, 2018 10:14 am

CKinnard wrote:The issue with reversing diabetes is any Calorie deficit can normalize blood glucose within 2 days. There are many studies from the WFPB and LC camps that don't control for weight loss (or the other factors mentioned in my earlier post) when examining effect on diabetes.

So what you're saying is that if you don't control of Cal deficit and therefore weight loss, that you can't draw any firm conclusions about whether a particular fat is a big factor or not. Fair enough. It's going to be harder to remove the fat and maintain the weight. A factor that usually isn't the goal of researchers, or diet study subjects either.

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Re: Diet Thread

Postby CKinnard » Mon Oct 22, 2018 11:23 am

Nobody wrote:So what you're saying is that if you don't control of Cal deficit and therefore weight loss, that you can't draw any firm conclusions about whether a particular fat is a big factor or not. Fair enough. It's going to be harder to remove the fat and maintain the weight. A factor that usually isn't the goal of researchers, or diet study subjects either.


When I started taking the LC camp more seriously, I could see their experience and later their studies showed the WFPB camp's truisms were flawed. i.e. Barnard, McDougall, Klaper, and many others were parroting for over a decade that fat causes insulin resistance and T2D by blocking insulin signaling on cell membranes via GLUT4 receptors. If this was the absolute truth, a high fat Calorie deficit diet, in which fat intake was higher than on a pre-existing isocaloric diet, would not result in blood glucose normalization. But these diets do reverse insulin resistance and lower blood glucose. This was known since the 70s when Atkin's diet was a thing.

The WFPB camp were one eyed, interpreting some of the literature and ignoring other observations and studies. The WFPB gurus persisted with this false paradigm many years after the literature made it abundantly clear they should not.

When I got into WFPB HQ (Santa Rosa) where McDougall and TNH are, I was reminded humans are very human. (I found the same thing in academia at Uni of Qld). The gurus anchor themselves in their paradigms, and deny or downplay any evidence that contradicts their constructs. Do I think less of them for this? No not really. I think we all do the same so as to be able to move forwards with confidence.
I do think those dallying in science and medicine should be less prone to this, but as I said if you are not reading 10+ hours a week, it is difficult to keep your perspective fluid and less peppered with uncertainty and contradictions. I also think until you are aware of the pervasiveness of human shortcomings, you are more inclined to inappropriately sanctify particular individuals.

So to answer your query, it is absolutely imperative to control all confounding variables in any study.
But to do so, you have to be aware of all confounding variables.
This is why I think one has to be aware of relying on reductionist studies that look at one aspect (biochem cascade or path) at a time, and attempt to infer a global effect. It is also why I think one has to weight larger studies like AHS II, EPIC Oxford, and systematic comparative observational studies such as Blue Zones and their spin offs (see below). When you are dealing with a complex system with tens of thousands of variables, it is helpful to stand back and look for patterns not visible with head in the trees. Reductionism is more likely to swing back and forth in perspective every time some new study puts a different spin on a subject. Whereas, the Blue Zone studies will still be as accurate in outcome, in 50 years as today.



https://www.ncbi.nlm.nih.gov/pubmed/17986602
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4241350/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3051199/
https://www.ncbi.nlm.nih.gov/pubmed/19948776/
https://www.ncbi.nlm.nih.gov/pubmed/18426957

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Re: Diet Thread

Postby mikesbytes » Mon Oct 22, 2018 2:18 pm

CKinnard wrote:yep n- 6:3 ratio is important due to the competition between both FAs to use the same enzymes to be reduced to usable form.
A high n-6 intake reduces n-3 conversion rate. which I mentioned in that other thread

Sorry to bring this back, as you guys have moved on. What's n-3 conversion rate? I though I read that n-3 needs to be ingested as the body doesn't produce it. Does the body need to create something else from the n-3 or am I completely confused?
If the R-1 rule is broken, what happens to N+1?

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Re: Diet Thread

Postby Nobody » Mon Oct 22, 2018 3:34 pm

mikesbytes wrote:
CKinnard wrote:yep n- 6:3 ratio is important due to the competition between both FAs to use the same enzymes to be reduced to usable form.
A high n-6 intake reduces n-3 conversion rate. which I mentioned in that other thread

Sorry to bring this back, as you guys have moved on. What's n-3 conversion rate? I though I read that n-3 needs to be ingested as the body doesn't produce it. Does the body need to create something else from the n-3 or am I completely confused?

That is somewhat like a "how long is a piece of string" question. The n-3 conversion rate depends if a person is male or female, what age, what their n-6:n-3 intake is like, what their conversion genes are like and what illness they may or may not have.

Have a read of this article and you'll see what I mean.
https://www.todaysdietitian.com/newarch ... 0p22.shtml
Last edited by Nobody on Mon Oct 22, 2018 4:39 pm, edited 1 time in total.

CKinnard
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Re: Diet Thread

Postby CKinnard » Mon Oct 22, 2018 4:07 pm

mikesbytes wrote:
CKinnard wrote:yep n- 6:3 ratio is important due to the competition between both FAs to use the same enzymes to be reduced to usable form.
A high n-6 intake reduces n-3 conversion rate. which I mentioned in that other thread

Sorry to bring this back, as you guys have moved on. What's n-3 conversion rate? I though I read that n-3 needs to be ingested as the body doesn't produce it. Does the body need to create something else from the n-3 or am I completely confused?


Poly unsaturated Omega-3 fatty acids are : ALA, EPA, and DHA
Mammals cannot synthesize any of these from scratch, though they are essential for many physiological processes....hence why they are called 'essential fatty acids'.

ALA is referred to as a short chain FA, having 18 carbons, and the other two are long chain and are most important functionally in mammals, including humans (EPA = 20 carbons, DHA = 22 carbons).

Mammals can convert dietary ALA into EPA, and EPA into DHA.
The conversion rates are highly variable depending on diet, genetics, and disease.
Recall I said earlier a high intake of n-6 can lower the conversion of ALA to EPA to DHA.
And in the Brenda Davis article Nobody linked to, all forms of fat can lower conversion rates.

The easiest n-3 dietary source on WFPB is ALA (many nuts and seeds); hence why the conversion rates to EPA and DHA are important if not taking supplements of these.

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Re: Diet Thread

Postby Nobody » Mon Oct 22, 2018 6:23 pm

CKinnard wrote:This is why I think one has to be aware of relying on reductionist studies that look at one aspect (biochem cascade or path) at a time, and attempt to infer a global effect...When you are dealing with a complex system with tens of thousands of variables, it is helpful to stand back and look for patterns not visible with head in the trees. Reductionism is more likely to swing back and forth in perspective every time some new study puts a different spin on a subject. Whereas, the Blue Zone studies will still be as accurate in outcome, in 50 years as today.

Yes in this case I appear to be the victim of reductionistic thinking brought on by some videos from thefruitdoctor which I posted in the other thread. I suppose like many of us, she is trying to find the ideal diet for herself and her clients/readers/watchers. Because nuts appear to increase LDL for an individual of her particular tested genetics and fats appear to affect her husband's T2D. I can therefore see why she ended up where she has. An easy trap to fall into.
However I'll continue to keep my fat around the 0.3 g/kgBW - down from the 0.4+g/kgBW - for a while and then get a blood test to see if it makes any difference to either my fasting BG or LDL-C. I suspect from past tests it won't, but I want to be sure.
So far I seem to feel more awake on lower fat, but it's a marginal change.

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Re: Diet Thread

Postby Nobody » Mon Oct 22, 2018 10:16 pm

For those interested in all things diet/weight_loss and not worried about not really learning anything. Then this average doco might be something to play in the background while doing more important things.

https://www.sbs.com.au/ondemand/video/1339319875630/the-diet-testers

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Re: Diet Thread

Postby CKinnard » Tue Oct 23, 2018 2:16 pm

Nobody wrote:Yes in this case I appear to be the victim of reductionistic thinking brought on by some videos from thefruitdoctor which I posted in the other thread. I suppose like many of us, she is trying to find the ideal diet for herself and her clients/readers/watchers. Because nuts appear to increase LDL for an individual of her particular tested genetics and fats appear to affect her husband's T2D. I can therefore see why she ended up where she has. An easy trap to fall into.


I had a look at another video she posted talking about her omega fa results.



She does not appear to be aware of the pitfalls of comparing FA tests of whole blood (includes plasma concentrations). These reflect very acute changes in diet, time of day, emotional state, etc.

To track the effect of diet manipulation more reliably, she should be using RBC and dried blood spot tests.
The difference is comparable to the diff between tests of plasma glucose vs A1c.
The FA results that are more meaningful are the concentrations in tissue, in this case RBC membranes....and not highly variable plasma concentrations.
And similar to A1c testing, FA testing of RBC is only meaningfully compared at least 2 months apart, due in part to the average 120 day lifespan of RBCs.

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Re: Diet Thread

Postby mikesbytes » Tue Oct 23, 2018 9:33 pm

Heard on the radio about plastic being found in human faces. While its a small sample of 8, each are from different countries and all 8 tested positive. A larger test would determine how common it is and the quantities. The article states its unknown what the effect on humans is

https://www.businessinsider.com.au/plastic-accumulates-in-human-feces-evidence-shows-for-first-time-2018-10?r=US&IR=T
If the R-1 rule is broken, what happens to N+1?

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Re: Diet Thread

Postby Nobody » Wed Oct 24, 2018 9:23 am

CKinnard wrote:...She does not appear to be aware of the pitfalls of comparing FA tests of whole blood (includes plasma concentrations). These reflect very acute changes in diet, time of day, emotional state, etc...

Thanks for the info.
I did my first dried blood spot method back on 13th March. Time has gotten away from me. I should get the second test done. If she had a spreadsheet like mine, she'd know exactly what her omega intake ratio was and how easy it is to get wrong. My daily omega 6:3 ratio is about 1.4:1 currently. I doubt I can get it lower unless I want delete the Brazil nut and supplement selenium. Or increase my 12 g/d linseed intake. Plus although the minimum intake for LA is unclear according to the WHO, they site 2% of Cal being adequate intake. I'm at that 2% limit. So along with the DHA supplement I'm expecting an improved result in my next test.

She is still learning with B12. Considering the non-linear absorption rates of B12, 5000 mcg once a week is the wrong way to do it. As in the frequency is more important than the dose. I found that 1000 mcg even 3 times a week wasn't enough for me. Daily 1000 mcg is ample for me, although it may not be enough for everyone. I considered dropping the dose and taking it twice daily. But since I can barely remember to take it every day currently, I doubt I'll remember twice daily.

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Re: Diet Thread

Postby Nobody » Wed Oct 24, 2018 9:45 am

mikesbytes wrote:Heard on the radio about plastic being found in human faces. While its a small sample of 8, each are from different countries and all 8 tested positive. A larger test would determine how common it is and the quantities. The article states its unknown what the effect on humans is

https://www.businessinsider.com.au/plastic-accumulates-in-human-feces-evidence-shows-for-first-time-2018-10?r=US&IR=T

Thanks for posting.
I would hope to have less than the average amount of plastic intake. But I'd be fooling myself to think I have none. I try to avoid plastic wrapped, canned and processed foods. But I still eat frozen foods that come in plastic bags. I rinse them, but I doubt that would have much effect. I also use the clear plastic bags when I buy fresh food at the supermarket. The bins that they come in are also plastic. The reusable bags I bring the food home in are plastic. Plastic is ubiquitous.
To me there is no surprise that the cancer rates are so high. We live in a highly artificial environment full of chemicals and toxins. Then eat a diet that is complicit with cancer growth.

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Re: Diet Thread

Postby CKinnard » Wed Oct 24, 2018 12:10 pm

Nobody wrote:Thanks for the info.
I did my first dried blood spot method back on 13th March. Time has gotten away from me. I should get the second test done. If she had a spreadsheet like mine, she'd know exactly what her omega intake ratio was and how easy it is to get wrong. My daily omega 6:3 ratio is about 1.4:1 currently. I doubt I can get it lower unless I want delete the Brazil nut and supplement selenium. Or increase my 12 g/d linseed intake. Plus although the minimum intake for LA is unclear according to the WHO, they site 2% of Cal being adequate intake. I'm at that 2% limit. So along with the DHA supplement I'm expecting an improved result in my next test.

She is still learning with B12. Considering the non-linear absorption rates of B12, 5000 mcg once a week is the wrong way to do it. As in the frequency is more important than the dose. I found that 1000 mcg even 3 times a week wasn't enough for me. Daily 1000 mcg is ample for me, although it may not be enough for everyone. I considered dropping the dose and taking it twice daily. But since I can barely remember to take it every day currently, I doubt I'll remember twice daily.


I respect her for her methodical approach, but get the impression she does everything alone, which can be tough. There's advantages in being part of a group of health professionals or avid enthusiasts, such as getting outside your own cognitive biases, and accelerating learning.
I find many who are motivated to micro-manage their nutrition got that way due to health issues.


Most leafy greens have a high portion of Omega 3, especially as the ratio n-3 : total Calories.
https://nutritiondata.self.com/foods-01 ... 000-1.html
The older I get, the more I appreciate the need to smash the vege. They are the most nutrient dense foods available.
And the more it makes sense that animals even carnivores, eat grass and green leaves when unwell.


I think the surest way to improve a dietary omega ratio is to

1. eat more leafy greens

2. don't overdo anything else (grains, legumes, and even walnuts...these all have at least 3-4x the n-6 to n-3, in addition to other forms of fat that compromise n-3 conversions.
https://en.wikipedia.org/wiki/Ratio_of_ ... rent_foods

And I appreciate you already do 1kg of fibrous carbs.
A major reason I've sowed a lot of leafy greens seeds since getting home is to up my intake of fresh green leaves.
__________

Yes, I agree re B12 supplements being taken in smaller doses more regularly.
I buy 1000mcg tablets, but cut them in half and do 500mcg most days.
I have considered cutting them in quarters and having a piece for brekky and dinner.......but too hard.
Actually something I've only just thought about is whether there's value in chewing B12 tablets, considering they benefit from binding to salivary R factor.

There's two transport systems to get B12 from the ileum into the blood
- binding to gastric originating intrinsic factor, for absorption in the ileum. This has an average peak B12 absorption capability of 2mcg/meal.
- passive absorption in the ileum, which is only about 1-3% efficient per meal.
- oral absorption is still disputed afaik.

B12 absorption is sensitive to binding to R factor (transcobalamin) in the saliva to endure the acid environment of the stomach.
An excessively acidic stomach environment will compromise B12 absorption.
Intrinsic Factor production decreases with age. So eating in a relaxed state, well hydrated, and chewing food adequately to mix with saliva, all benefits B12 digestion and absorption.

The above favor taking smaller doses more frequently.

Finally, a study I read a few weeks ago reasoned that there are colon bacteria that can synthesize B12, but as we know, B12 cannot be absorbed here. However, it may be that a healthy high population of the right colon bacteria migrates somewhat into the ileum, where B12 can be absorbed.

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Re: Diet Thread

Postby mikesbytes » Wed Oct 24, 2018 9:28 pm

Nobody wrote:
mikesbytes wrote:Heard on the radio about plastic being found in human faces. While its a small sample of 8, each are from different countries and all 8 tested positive. A larger test would determine how common it is and the quantities. The article states its unknown what the effect on humans is

https://www.businessinsider.com.au/plastic-accumulates-in-human-feces-evidence-shows-for-first-time-2018-10?r=US&IR=T

Thanks for posting.
I would hope to have less than the average amount of plastic intake. But I'd be fooling myself to think I have none. I try to avoid plastic wrapped, canned and processed foods. But I still eat frozen foods that come in plastic bags. I rinse them, but I doubt that would have much effect. I also use the clear plastic bags when I buy fresh food at the supermarket. The bins that they come in are also plastic. The reusable bags I bring the food home in are plastic. Plastic is ubiquitous.
To me there is no surprise that the cancer rates are so high. We live in a highly artificial environment full of chemicals and toxins. Then eat a diet that is complicit with cancer growth.

Aside from the question as to whether the ingested plastic is harmful or not, I guess the question is to under what circumstances are resulting in ingested plastics. The answer to that question could change some of our habits. I'm suspecting that heating plastics, such as in the microwave are releasing the plastics into the food, however I have zero scientific data to backup/repute my assumption

In regards to cancer I heard today about the link between obesity and cancer. Something we already knew. I suspect this is a much bigger issue than plastic
If the R-1 rule is broken, what happens to N+1?

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Re: Diet Thread

Postby Nobody » Thu Oct 25, 2018 8:17 am

CKinnard wrote:I think the surest way to improve a dietary omega ratio is to

1. eat more leafy greens

2. don't overdo anything else (grains, legumes, and even walnuts...these all have at least 3-4x the n-6 to n-3, in addition to other forms of fat that compromise n-3 conversions.
https://en.wikipedia.org/wiki/Ratio_of_ ... rent_foods

And I appreciate you already do 1kg of fibrous carbs.
A major reason I've sowed a lot of leafy greens seeds since getting home is to up my intake of fresh green leaves.


1. Good general advice, especially if trying to keep the Cal density low. We both post in reply, but also keeping in mind the general audience. In my case I find I have to consider the benefit versus added iron. When it comes to green leafy, then most think of English spinach, rocket and kale. For ALA intake versus iron, linseed is still a better choice for me. Some foods just aren't worth it if you have a particular condition. My experience has hopefully shown that foods higher in iron, of say over 1g/100g should be limited if one has iron_loading/haemo issues. All listed above have at least 1.5, with spinach being 2.7.

2. Agree. I've reduced the nuts and grains. Feeling more awake since the change, but I might be more irritable/emotional (marginal and a subjective observation in a changing environment). I thought my skin would become drier, but I haven't noticed much - if any - change. Legumes have always messed with me (short and longer term), so I'm happy not to try them again. Iron content is high too.
I'm getting the impression that the ideal ratio closer to 1:1 than 2:1. Not easily achievable without extremes, but worth moving toward. I was 1.2:1 yesterday, but that was also a 1609 Cal day (too busy to eat).

mikesbytes wrote:...I guess the question is to under what circumstances are resulting in ingested plastics. The answer to that question could change some of our habits. I'm suspecting that heating plastics, such as in the microwave are releasing the plastics into the food, however I have zero scientific data to backup/repute my assumption

I don't use the microwave to heat or defrost anymore. Favouring running cold water to do the job instead. Obviously people can avoid plastic my moving into ceramic bowls with a plate on the top. However, when it comes to food preparation, laziness is the modern norm.

mikesbytes wrote:In regards to cancer I heard today about the link between obesity and cancer. Something we already knew. I suspect this is a much bigger issue than plastic

I would have thought that obesity is more another symptom, rather than a major cause in itself. The western diet eating style being the major cause of cancer growth. However obesity in itself could be causative. Since cancer is also considered to stem from an inflammatory condition and there is more of it with obesity.

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Re: Diet Thread

Postby CKinnard » Thu Oct 25, 2018 10:56 am

Nobody wrote:1. Good general advice, especially if trying to keep the Cal density low. We both post in reply, but also keeping in mind the general audience. In my case I find I have to consider the benefit versus added iron. When it comes to green leafy, then most think of English spinach, rocket and kale. For ALA intake versus iron, linseed is still a better choice for me. Some foods just aren't worth it if you have a particular condition. My experience has hopefully shown that foods higher in iron, of say over 1g/100g should be limited if one has iron_loading/haemo issues. All listed above have at least 1.5, with spinach being 2.7.


Something doesn't intuitively gel for me re reducing leafy greens for iron overload pathology.
I know that challenges convention++, but I haven't found any study that has comprehensively investigated the issue i.e. via a dose sensitive study of leafy greens and transferrin/ferritin levels.

So why am I suspect on this issue?
- Leafy greens have high levels of calcium, an iron absorption inhibitor.
- Spinach has high levels of oxalate, another iron absorption inhibitor.
- Oxalate also inhibits the absorption of calcium, leading to higher levels of calcium in the small intestine, which hypothetically should inhibit iron absorption more so.
- Leafy greens are high in fiber, which inhibits iron absorption.
Indeed, the reputable 'Iron Disorders Institute' recommends the intake of spinach for iron overload diseases.
http://www.irondisorders.org/Websites/i ... ations.pdf

- Leafy greens are among the very highest dietary source of anti-oxidants, and have the highest ratio of anti-oxidants per Calorie.
It is very plausible that leafy greens' anti-oxidant effect on iron's destructive oxidative capabilities, results in a net therapeutic effect of high leafy green intake.

Phytates are one of the most powerful inhibitors of iron absorption. And I think a balance WFPB diet will contain reasonable quantities of these.

________________

Some reading that contradicts convention:


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2657669/
Can J Gastroenterol. 2007 Feb; 21(2): 101–104.
The myths and realities of hemochromatosis
Melanie D Beaton, MD and Paul C Adams, MD

"Hemochromatosis patients should be on a low-iron diet

Although dietary iron is the source of excess iron in hemochromatosis, a decrease in dietary iron has not been shown to decrease iron stores in hemochromatosis. All food groups contain iron and most humans will absorb only a small fraction of orally ingested iron. Iron absorption includes components from heme and nonheme iron sources (22), and the control or lack of control over these regulatory mechanisms is incompletely understood in hemochromatosis. It has been speculated that a defect in hepcidin, a circulating peptide produced by the liver, is a fundamental defect in hemochromatosis which results in an increase in intestinal iron absorption (23). Iron supplementation of food was introduced in the 1950s as a marketing tool, and the added iron has poor bioavailability. Generally, vegetarians have lower serum ferritin levels than meat-eating patients but this does not translate into a dietary recommendation (24). The description of bacterial infections from Yersinia (25) and other Vibrio species has led to recommendations to avoid raw shellfish which may be appropriate for all patients rather than just hemochromatosis patients. Hemochromatosis patients are advised to avoid iron supplementation and large doses of supplemental oral vitamin C which may adversely affect some patients with iron overload (26)."
________________


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3378281/
Can J Gastroenterol. 2012 Jun; 26(6): 345–349.
Dietary iron intake and serum ferritin concentration in 213 patients homozygous for the HFEC282Y hemochromatosis mutation
Victor R Gordeuk, MD, et al

Abstract
BACKGROUND:

HFEC282Y homozygotes have an increased risk for developing increased iron stores and related disorders. It is controversial whether dietary iron restrictions should be recommended to such individuals.
OBJECTIVE:
To determine whether dietary iron content influences iron stores in HFEC282Y homozygotes as assessed by serum ferritin concentration.
DESIGN:
Serum ferritin concentration was measured and a dietary iron questionnaire was completed as part of the evaluation of 213 HFEC282Y homozygotes who were identified through screening of >100,000 primary care patients at five HEmochromatosis and IRon Overload Screening (HEIRS) Study Field Centers in the United States and Canada.
RESULTS:
No significant relationships between serum ferritin concentration and dietary heme iron content, dietary nonheme iron content or reports of supplemental iron use were found.
CONCLUSION:
These results do not support recommending dietary heme or nonheme iron restrictions for HFEC282Y homozygotes diagnosed through screening in North America.

RhapsodyX
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Re: Diet Thread

Postby RhapsodyX » Thu Oct 25, 2018 2:40 pm


Nobody
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Re: Diet Thread

Postby Nobody » Thu Oct 25, 2018 10:11 pm

CKinnard wrote:Something doesn't intuitively gel for me re reducing leafy greens for iron overload pathology.
I know that challenges convention++, but I haven't found any study that has comprehensively investigated the issue i.e. via a dose sensitive study of leafy greens and transferrin/ferritin levels...

Image

Pick which block I added an average of 80 g/d of English spinach without changing anything else about my diet or lifestyle. The answer is easy to pick, isn't it? Although I wouldn't say that no other studies matter. This anecdote obviously is more relevant to me than any of them.

Sometimes smart people with lots of letters after their name aren't the most logical thinkers. Like my specialist who told me that diet doesn't make any difference to haemo. Which her own department head didn't agree with I was informed. Obviously it makes no difference to the cause, but it seemed to make a difference to the results and still does. She was the same one who appeared to get hostile after I mentioned I was vegan. She said she was vegetarian. Every time I went back to see her she was bigger. But to her, I was the fool. Oh well, some people are just too smart to learn anything new. [Obviously no implication intend toward you CK. :) ]

CKinnard
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Re: Diet Thread

Postby CKinnard » Thu Oct 25, 2018 11:16 pm

Nobody wrote:

Pick which block I added an average of 80 g/d of English spinach without changing anything else about my diet or lifestyle. The answer is easy to pick, isn't it? Although I wouldn't say that no other studies matter. This anecdote obviously is more relevant to me than any of them.

Sometimes smart people with lots of letters after their name aren't the most logical thinkers. Like my specialist who told me that diet doesn't make any difference to haemo. Which her own department head didn't agree with I was informed. Obviously it makes no difference to the cause, but it seemed to make a difference to the results and still does. She was the same one who appeared to get hostile after I mentioned I was vegan. She said she was vegetarian. Every time I went back to see her she was bigger. But to her, I was the fool. Oh well, some people are just too smart to learn anything new. [Obviously no implication intend toward you CK. :) ]


Yes, I did remember you had self experimented previously.
I'd be very interested to see you repeat the trial, and maintain it for at least 6 months, no blood draws.
But it's your body! :)
213 subjects above didn't demonstrate the same effect!!!
I presume it takes some time for the body to adapt to a higher intake.

Nobody
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Re: Diet Thread

Postby Nobody » Fri Oct 26, 2018 7:39 am

CKinnard wrote:213 subjects above didn't demonstrate the same effect!!!

That's the beauty of self experimentation. Those 213 subjects weren't me. Technically I don't even have haemo by genetics. It comes back hetero-zygote. But I appear to have the same symptoms and respond to the same treatment, so that's all that matters at this stage. Maybe my specialist was right. In that diet change doesn't effect real genetic haemo patients. But it does effect me. Which in that case I'm the fortunate one because I can get results others can't. Although I'm still no better off than the average haemo sufferer because I'm still on regular 6 monthly bleeds. I hear some others get to regular annual bleeds. Which I only managed once.

Moving forward I'm only interested in doing self experiments that may benefit my health. On reflection, I must have been crazy to do it the first time. I'm glad it didn't last 6 months. I've proved that point to myself. I'm still self experimenting with DHA and calcium supplementation at the moment and a bit concerned they may be doing more harm than good.

CKinnard wrote:I presume it takes some time for the body to adapt to a higher intake.

Could it be a saturation problem? They are getting so much absorb-able (heme) iron that the extra doesn't make a difference. Similar to the cholesterol studies that show no effect.

CKinnard
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Re: Diet Thread

Postby CKinnard » Fri Oct 26, 2018 8:50 am

Nobody wrote:Could it be a saturation problem? They are getting so much absorb-able (heme) iron that the extra doesn't make a difference. Similar to the cholesterol studies that show no effect.


I haven't read the full paper, so don't know the methods. I looked for it unsuccessfully because I was interested to know the duration.

One of my lecturers that I highly respected made a good point, that more scientific studies need to be repeated. It's a serious side of determining reliability.

Do I do recall correctly you were hetero-, not homo-zygote, at least for the mutations tested?

Anyway, I am not playing devil's advocate. I have just seen too many incidences in medicine where concrete positions are taken with nothing approaching an adequate evidence base.

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Re: Diet Thread

Postby Nobody » Fri Oct 26, 2018 2:06 pm

CKinnard wrote:One of my lecturers that I highly respected made a good point, that more scientific studies need to be repeated. It's a serious side of determining reliability.

True, but there's no money for it when they think they have the answer. Many studies these days are industry funded mock ups to make something look good. Unless government want to spend money on fact checking, the repeats probably won't happen.

CKinnard wrote:Do I do recall correctly you were hetero-, not homo-zygote, at least for the mutations tested?

Correct. Of course the test could also be incorrect. It wasn't repeated either. What is does say on the test:
Moderately increased ferritin is is common in C282Y, H63D or S65C heterozygotes but iron overload is unlikely. Iron overload is rare in H63D or S65C homozygotes.

I'm H63D. So whether homo or hetero, it's rare to have iron loading. I'm rare apparently. But I could have told you that before the test. :wink:

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