Plant Based Diet Thread

[Nobody]

Most of the people I have known who had high blood pressure were obese or heading that way. Could be due to high consumption of manufactured foods resulting in high salt consumption or due to the weight itself.

High BP is usually a long term result of eating a standard diet. AFAIK GPs expect the average western man's systolic BP to rise a 1mm of mercury a year. So by 40 yo, it is expected that those susceptible will be on medication by then because their systolic BP is 140. I know quite a few who are.

Body weight is a factor, which is interesting in my case. Since I'm heavier than I have been in the last few years, yet my BP is lower.

[CKinnard]

Body weight is a factor, which is interesting in my case. Since I'm heavier than I have been in the last few years, yet my BP is lower.

Bodyweight is only a BP issue when it is fat, because the fatter you are the more fat you store ectopically in arteries.
If you increase muscle mass, and do moderate cardio, you increase the cross sectional area of arterioles in the body via capillary sprouting.
This has the most powerful effect of any intervention on lowering BP.

[Nobody]

Thanks CK. Interesting. I'll have to confirm my BP with the GP in Jan. At least it gives me some more inspiration to do some dead lifts.

[CKinnard]

Thanks CK. Interesting. I'll have to confirm my BP with the GP in Jan. At least it gives me some more inspiration to do some dead lifts.

remember the HIIT and moderate intensity enduro. Together with the resistance stuff, they are the best stimulus for capillary sprouting.

I am surprised you don't have a BP machine at home. A $40 unit is very reliable these days.
I talked to a guy at TNH this year about pros/cons of domestic market ECG. The cheapest units are now under $1000.
Self monitoring ecg would actually save more lives than self monitoring BP.
Though the algos for interpreting signal still need improvement.
Was talking with local ambos at coffee this week, and their new 12 lead portable ecg computer interpretation is as shoddy as 15 years ago.
Totally inexcusable.

[Nobody]

Remember the HIIT and moderate intensity enduro. Together with the resistance stuff, they are the best stimulus for capillary sprouting.

OK, thanks.

I am surprised you don't have a BP machine at home. A $40 unit is very reliable these days.

I've relied on hospitals or GPs so far because they are considered trustworthy references. Also BP usually changes very slowly for people like us and up until now I've only been interested in the long term trend.

____________________________________________

On the surface, it looks like the grain producers of the world are fighting back against the low carb movement.

Article:
http://www.smh.com.au/lifestyle/health- ... zzr39.html
Organisation:
http://carbquality.org/
http://www.gisymbol.com/international-c ... onsortium/
Their paper:
http://www.nmcd-journal.com/article/S09 ... 0127-1/pdf

[Nobody]

Below is a plant based success story. Her cholesterol went from 6.6 to 3.9 and hsCRP went from 4.17 to 1.49. Probably an excellent result for someone with type 1 diabetes.
She says anything below 1 is "no risk". But according to the AHA article (below), it's just lower risk. No added risk with a relative risk score of 1 is for people with a hsCRP result below 0.5.


http://circ.ahajournals.org/content/109/16/1955.full

[Nobody]

I found the below article particularly interesting as it attempts to overturn the current conventional wisdom that higher omega-6 fats are bad for your inflammation levels.

Omega-6 fatty acids do not promote low-grade inflammation

The higher the serum linoleic acid level, the lower the CRP, according to a new study. Linoleic acid is the most common polyunsaturated omega-6 fatty acid.

Study Abstract

Conclusions
Serum n-6 PUFAs were not associated with increased inflammation in men. In contrast, the main n-6 PUFA linoleic acid had a strong inverse association with the key inflammation marker, CRP.

___________________________________________________________

Article below is on nut consumption and incidence of events associated with atherosclerosis. Although not new, it reinforces the evidence of nuts with arterial health. Just keep in mind that Jeff Novick showed that the better your diet is, the less benefit one gets from added nuts. So no point overdoing it as nuts can add weight for at least some individuals. I currently eat about 8 to 12g of nuts per day. I also eat 10 to 12g of linseed.

Eating regular variety of nuts associated with lower risk of heart disease

[Tim]

Not particularly relevant to anything but I eat 1 - 1.5 kg's of unsalted cashews, almonds (and peanuts) per week and have been doing so for about the last eight years.
This is combined with at least 10 daily serves of fruit and veg, usually more at 15+.
In between breakfast and dinner I eat little else other than fruit and nuts and maybe a wholemeal/grain salad sandwich with or without tuna and cheese. I graze constantly ie. snacking hourly.
Weight has remained steady at between 61-64 kg's since I was 16yo (nearly 40 years).
My weight has recently dropped down to 61kg's as a result of reduced refined sugar (ice cream, chocolate, homemade shortbread) intake and increased high(ish) intensity criterium cycle race training over a 12 week period. Training about 7 - 14 hours a week. Exercise weekly calorie burn is up to about 4000 calories although this is a very rough figure.
Cooked porridge (0.25 cup raw oats, 0.5 - 0.75 cup raw oat bran) for breakfast with heaped tablespoon honey and sometimes dates or other fruit such as strawberries, kiwifruit, banana etc.
Some red meat, small 100gram portions 2-3 days/week, chicken or seafood other nights in higher quantity than red meat.
Pasta, rice (white), grains, legumes, pulses, good quality wholemeal breads if not daily at least weekly.
I don't consciously exclude anything from my diet but do restrict saturated fats, red meat, junk food, highly processed food and refined sugar at times.
I'm trying hard not to preach, sound smug or annoy, but a lifetime of eating this way seems to work for me. All general health indicators (BP, cholesterol etc.) are good. The only health issues I've ever faced have been relatively mild sport, physical work and age related joint wear and tear. Lifestyle/sun related skin and eye cancer though no worse than BCC level and intermittent and fairly mild anxiety/depression type problems. All of which can usually be overcome with a little dedicated diet, exercise or attitude improvement.

Edit; I just realised this post should be in the diet thread but then again my diet is basically plant based with a small amount of supplementary animal produce such as cheese, yoghurt, milk, eggs and meat. On average I'd probably eat one of the above each day, but again in comparatively small amounts. I rarely measure or weigh anything.

[march83]

@Nobody: does the study relate serum o6 and dietary o6?

[Nobody]

@Nobody: does the study relate serum o6 and dietary o6?

Good point and thanks for pointing it out. Sorry, looks like I misread it. It appears to be serum. I'll edit.

The study found that a low serum linoleic acid level was associated with higher serum CRP levels.

On reflection it's hard to relate to this study as no one usually gets their serum n-6 or linoleic acid (LA) levels tested. Do you know yours? I don't know mine. The abstract didn't show the average LA levels either.
I know that my normal hsCRP is ~0.5 mg/L (lowest group average in study was 1.37) yet I'd guess my LA levels would be low compared to the study participants. Just goes to show that there is more to inflammation than just serum fat levels. About a 18 months or more ago I tried to add more nuts to my diet, but my hsCRP didn't increase. So that appears to agree with the study results.

[CKinnard]

You want to be careful reading too much into this study.

- It is a recent statistical analysis on data collected 30 years ago.

- It uses a cut off of 3mg/L as the threshold for elevated CRP associated with increased disease risk, when 2mg/L is the current threshold.

- It uses CRP rather than hsCRP, the latter being a better indicator of "chronic" inflammation, which is more associated with cardiovascular risk. CRP indicates acute inflammation.

- Today, there are more sensitive markers of chronic inflammation and endothelial dysfunction : f2-iso-prostanes, dimethylarginine, myeloperoxidase. microalbumin.

[Nobody]

You want to be careful reading too much into this study.

Agree. That's why I said "attempts". Early days and since most don't know their LA levels, or what the people ate, it doesn't tell us a lot IMO. Just interesting.

- It uses a cut off of 3mg/L as the threshold for elevated CRP associated with increased disease risk, when 2mg/L is the current threshold.

Thanks. That's interesting too. In 2003 it was 3mg/L. When did it change? Gotta link? I might have a dig myself. I'm personally not big on cutoffs, since reality is an analogue sliding scale. I think people should just get as low as they can when it comes to hsCRP.

http://circ.ahajournals.org/content/108/12/e81.full

- It uses CRP rather than hsCRP, the latter being a better indicator of "chronic" inflammation, which is more associated with cardiovascular risk. CRP indicates acute inflammation.

To show my ignorance, other than the range it measures to, what is the difference? I have a CRP result posted here which showed "< 3".

- Today, there are more sensitive markers of chronic inflammation and endothelial dysfunction : f2-iso-prostanes, dimethylarginine, myeloperoxidase. microalbumin.

If you ask your GP, can you easily get any/all of these in a blood test?

[march83]

Is there a simple way to get a CRP blood test? Do you just need to find a friendly GP

[Nobody]

Is there a simple way to get a CRP blood test? Do you just need to find a friendly GP

It appears to depend on your age somewhat. At 40+ yo it appears easy since your risk is considered high.

_____________________________________________________

OK CK. I had look and found a more recent AHA article from 2010 which showed hsCRP of 2 is the cutoff and why. Below is a mock up of what is found in the article's "Figures and Tables" section.

[Relative Risks] of CV events:_____________________________Value______Range
Men:
    RR of CV events resulting from hs-CRP ≥2.0______1.18______1.06–1.30
    RR of CV events resulting from hs-CRP <2.0______0.90______0.81–0.99
women:
    RR of CV events resulting from hs-CRP ≥2.0______1.15______1.04–1.27
    RR of CV events resulting from hs-CRP <2.0______0.83______0.75–0.91

http://circ.ahajournals.org/content/122 ... gures-data

I'll have a go at helping to make the numbers clearer for others reading:
A relative risk of no greater than normal is considered to be 1.
So any higher than 1 as a ratio is higher risk. So for example the 1.18 above would mean on average, 18% more men have CV events with hs-CRP >2.
So < 2.0 is lower than average risk and > 2.0 is higher. That is why 2.0 is now considered to be the threshold.

I find it interesting that in the Framingham AHA article posted earlier here, that they relative risk of 1 is for a hs-CRP of < 0.5. They must be very healthy people or they measure relative risk differently.

So USA MDs have now determined that 2.0 is average risk. But I'd prefer not to have the average risk, so I'm now going to cook some more veg...

[CKinnard]

The Jupiter study into appropriate prescription of statins was a large study that used 2mg/L.
Thresholds are a fluid thing, and your GP has probably told you hsCRP is of dubious benefit in changing disease mgt. If you want to knock yourself out ->
http://www.sciencedirect.com/science/ar ... 971302086X

I think the other markers I mentioned are better science because they more directly reflect CVD pathology, from the outset.

[Nobody]

There has been posting of links to say wheat can cause leaky gut and other stomach problems. The first half of this video appears to explain why. It doesn't appear to be the type of wheat, but the herbicides used and the way they are used.



The main study cited about Glyphosate:
https://www.degruyter.com/downloadpdf/j ... 3-0026.pdf

[Nobody]

The Jupiter study into appropriate prescription of statins was a large study that used 2mg/L.
Thresholds are a fluid thing, and your GP has probably told you hsCRP is of dubious benefit in changing disease mgt. If you want to knock yourself out ->
http://www.sciencedirect.com/science/ar ... 971302086X

I think the other markers I mentioned are better science because they more directly reflect CVD pathology, from the outset.

From the article you linked.

hsCRP continues to be tested routinely, despite its difficult and controversial value in guiding treatment decisions. The association between elevated hsCRP levels and CVD is well established. Further, the literature also modestly supports the incremental value that hsCRP may have to current risk prediction models. However, reclassification of intermediate-risk patients with the addition of hsCRP to existing FRS variables does not meaningfully alter clinical management. Last, there is inconclusive evidence that reducing hsCRP levels prevents CHD.

I think the crux of the article is above. It appears to be be saying it has merit, but not enough to alter clinical practice. Clinical practice looks at many risk factors and may include CAC and other tests. But for me, a person not in clinical practice, I still believe it has some value since I'm not going to get a CAC just to see if all is well.

As for the other markers you mentioned which are better. Which ones can you get measured through a simple blood test though your GP?

[CKinnard]

From the article you linked.

hsCRP continues to be tested routinely, despite its difficult and controversial value in guiding treatment decisions. The association between elevated hsCRP levels and CVD is well established. Further, the literature also modestly supports the incremental value that hsCRP may have to current risk prediction models. However, reclassification of intermediate-risk patients with the addition of hsCRP to existing FRS variables does not meaningfully alter clinical management. Last, there is inconclusive evidence that reducing hsCRP levels prevents CHD.

I think the crux of the article is above. It appears to be be saying it has merit, but not enough to alter clinical practice. Clinical practice looks at many risk factors and may include CAC and other tests. But for me, a person not in clinical practice, I still believe it has some value since I'm not going to get a CAC just to see if all is well.

As for the other markers you mentioned which are better. Which ones can you get measured through a simple blood test though your GP?

Other markers? Well I haven't made an exhaustive study, but took on board what Michael Klaper and Caldwell Esselstyn stand behind, and that's the Cleveland Heartlab protocol, which I think I've mentioned here before.
http://www.clevelandheartlab.com/wp-con ... 6i-web.pdf
I did a small search when I got back from US to see who might provide similar tests here. I think there was a lab in Melbourne that matched some. I think Australians have to accept we don't do much at the cutting edge of medical science, and we are probably too cynical about change. It isn't Medicare's role to be at the cutting edge, but to ensure ALL have a minimum standard of health care.

I thought the Scandinavians might have better public, and private insurer, health care than Australia, But I looked after 7 or 8 Scandos at True North who had been wrongly diagnosed and poorly managed at home.

The whole thing about CRP and hsCRP is if it elevated or if it is not, what health mgt options does it provide?
- lifestyle adjustment, primarily food and alcohol.
- statins

That's the way GPs look at it. Most of their workload is in getting people to modify lifestyle, so hsCRP has benefit over FRS which misleads people into believing their lifestyle is healthy enough.
But if you have already optimized lifestyle factors as you have mostly done Nobody, then hsCRP has little to add.
Further, hsCRP is purely inflammatory. It says nothing about insulin sensitivity and oxidative stress, the two others of the ugly triad most responsible for accelerated tissue and systems damage.

I am shortlisted to do a presentation at next year's Australasian Society of Lifestyle Medicine Convention in Brisbane. I should be among like mindeds there, and have a growing list of topics including earlier warning of CVD, that I want to discuss between presentations.

[Nobody]

Andrew did a low fat vs high fat experiment on himself with interesting results in regard to testosterone blood levels.
The comment by "nanook kernell" I thought was interesting. I've also found my sex drive to be low. But like "nanook", at my stage of life I prefer it.

The video:
https://youtu.be/j0Vkhm7tY7g

My fat intake has increased from about 7% to 9% in recent months (according to Cronometer), with an increase in weight. My skin is better for it though. I think I would need to restructure my diet and calorie restrict/IF to get to 15%+ fat without adding even more weight. I'll get back on the bike more and see how I'm fairing then.

[mikesbytes]

That's interesting nobody, I wouldn't of thought that fat would of made that much difference on hormone production, particularity on a male.

If I heard in right, he's targeting 15 - 20% of calories from fat for his normal diet?

[CKinnard]

hmmm....I am not a big fan of using libido as a health metric. After all, what are we talking about exactly? lust? sexual preoccupation? unsatisfied sexual hunger?

These are not positive attributes in my view. They distract one from focusing on higher hierarchical needs as indicated by Maslow's hierarchy. Many people with 'healthy libido' in the West become owned by it, at the expense of cultivating intellectual power, empathy, responsibility to family and community, personal growth.

The west focuses way too much on sex in the view of many including me. I think the more industrious and fulfilled one is in other areas of life, the less obsessed one is with sex drive.

From a purely biological perspective, sex is PRIMARILY for procreation, and I think it is totally appropriate that libido ease once one has children to mould into creative beings. Some argue against this, but they are denying the biology.

Further, what constitutes a 'healthy' libido is not consistent across the world. Asians in general are not as sex conscious as Westerners. And neither were our forebears. When one has a full work load to occupy them, sex takes more and more a back seat. So in some respects, sex plays more so in idle minds. I have found it true that the more constructively productive a person, the less they are troubled by sex drive.

I explored Eastern philosophies/religion (and Western) when younger, and spent a lot of time with yogis and monks. No matter their background, the truly genuine ones advised against engaging in sex for anything other than procreation. It's something I innately feel is right. However, I know that is draconian and goes against Western 'culture'.

In my view, the greatest expression of love is not making love, but helping another realize their full potential.
And basic trust and respect of the opposite sex is very much dependent on not sensing another's libido interferes with their cognitive and ethical qualities.

Anyway, sorry for the rant. It's not a judgement on others' views. I just see so much of Western civilization's issues relate very much to libido.

As for dietary fat, note the steroidogenic pathway which highlights all sex hormones originate from cholesterol.



Further, any physiological stress tends to dampen libido. acute pain is perhaps the strongest, dieting/fasting, significant life stressors. This is well explained in that we evolved only to reproduce when we had more basic survival needs met.

[Nobody]

If I heard in right, he's targeting 15 - 20% of calories from fat for his normal diet?

https://youtu.be/j0Vkhm7tY7g?t=3m48s

Yes, you heard correct. He does better with more fat. But as he said, there is no body of evidence showing that high levels of fat are as healthy as < 10% fat when it comes to atherosclerotic health. While Greger (nutritionfacts.org) will show evidence that nuts and seeds are beneficial, Esselstyn to my knowledge hasn't changed his stance from his book that says if you have heart disease, then no nuts. If you don't have heart disease, then have a few walnuts per day in addition to the 1 to 2 tbsp of linseed/flax daily. At the moment I follow Esselstyn's advice and have 12g of linseed, plus <= 10g walnuts daily. I don't go nuts with nuts because (despite the NutritionFacts evidence to the contrary) it appears to add weight for me, I already have high LDL cholesterol for what I eat (2.2 mmol/L) and my father has had 2 strokes already.

The problem we have is there aren't enough (independently funded) studies to show a higher fat plant only diet is as healthy as low fat for atherosclerosis, the microbiome and insulin sensitivity. Even the NutritionFacts videos show higher fat is bad for insulin sensitivity.

Another recent PCRM video which throws doubt on higher fat diets.

[Nobody]

hmmm....I am not a big fan of using libido as a health metric...Many people with 'healthy libido' in the West become owned by it, at the expense of cultivating intellectual power, empathy, responsibility to family and community, personal growth.

Agree. IIRC I think it was Campbell who wrote in one of his books that women in the US on average had a 50% longer fertility period compared with the rural Chinese women. That appears to suggest that western style diets are creating unnatural hormone levels. This will appear strange from the perspective of a normal westerner, but I find it's empowering to be largely free of the 'healthy libido'.

[CKinnard]

Following up on my previous post, like herbivores, humans do not need to eat any cholesterol whatsoever. Every human cell can synthesize it from basic, common metabolites....though the liver is the primary source.

A noteworthy extract re testosterone variation.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367619/

"Second, T can be seen as a mediator of life-history trade-offs, such as investment in self-maintenance (survival) versus reproduction or in allocating resources to mating versus parental care (Ricklefs & Wikelski 2002; Hau 2007). For example, high plasma T levels usually coincide with periods of intense male–male competition in the form of territory defence, access to females, paternity protection or sperm competition, whereas low levels of T usually coincide with periods of paternal care (Wingfield et al. 1990; Pinxten et al. 2007). Thus, individual variation in the duration of elevated T levels may reflect variation in life-history strategies.

Two further issues are highly relevant for understanding the relationship between variation in T levels and phenotypic traits and are unfortunately often ignored by ecologists. They are highlighted elsewhere in this issue (Ball & Balthazart 2008) and we will only mention them briefly here. First, in the context of sexual selection theory, studies on the costs and benefits of maintaining high or low T levels usually assume a dose-dependent relationship between T and fitness-related traits. However, this relationship can have different forms and the evidence for dose dependency appears limited (reviewed in Hews & Moore 1997; Adkins-Regan 2005). In fact, variation in the duration of the period of elevated T might be more important to understand costs/benefits of T than variation in absolute T levels (see §2b). Second, as stressed by many endocrinologists, hormones are only part of the endocrine system and investigating them in isolation can lead to misleading conclusions (Dufty et al. 2002). Hormonal responses occur only if the appropriate receptors are available in or on the cell. Receptors can vary in number, affinity and specificity, and these properties might differ systematically among individuals (Adkins-Regan 2005; Ball & Balthazart 2008). Moreover, the number of receptors is not static, but can be up- and downregulated. Thus, the threshold at which T affects a trait can probably change within individuals, for example, through changes in receptor density in particular brain regions (Canoine et al. 2007). Finally, steroid hormones circulate mostly bound to proteins that increase their solubility in the blood. However, it is the unbound hormone that is biologically active. Thus, changes in plasma-binding protein levels will alter hormone availability without changing overall plasma hormone concentrations (Dufty et al. 2002; Ball & Balthazart 2008). In summary, the biological relevance of absolute plasma T levels may only be understood when considering variation in other aspects of individual T regimes."

[CKinnard]

hmmm....I am not a big fan of using libido as a health metric...Many people with 'healthy libido' in the West become owned by it, at the expense of cultivating intellectual power, empathy, responsibility to family and community, personal growth.

Agree. IIRC I think it was Campbell who wrote in one of his books that women in the US on average had a 50% longer fertility period compared with the rural Chinese women. That appears to suggest that western style diets are creating unnatural hormone levels. This will appear strange from the perspective of a normal westerner, but I find it's empowering to be largely free of the 'healthy libido'.

Yes, I think it is a consideration that is worth noting, that as a man ages, and is more likely to become a teacher of younger gens, that his libido decrease, and his sense of civic duty and paternal care increase. If society has gone to the dogs in the last 40 years, it is very much due to my generation being self absorbed rather than caring enough about the health of community and nation.