CHD etiketine sahip kayıtlar gösteriliyor. Tüm kayıtları göster
CHD etiketine sahip kayıtlar gösteriliyor. Tüm kayıtları göster

4 Aralık 2015 Cuma

Low-carbohydrate High-fat diets: Green flags and Red flags.

Fun with flags. But first, a poem!

Atkins Antidote


Eating low carbohydrate what threat that poses

Do my friends think I’m suffering from halitosis?

I’ve got these sticks for measuring ketoacidosis

I’m taking supplements but I don’t know what the dose is

I’m trying hard to keep in a state of ketosis

I’m not sure what the right amount of weight to lose is

I’m sure I’ve put on a pound just through osmosis

Is eating this way risking osteoporosis

Are my kidneys wrestling with metabolic acidosis

My store of liver glycogen I don’t know how low is

Who knows what the glycemic load of oats is

Does anyone know if I can eat samosas?



Ian Turnbull


I do. The answer's "No!" :-D
From https://forum.nationstates.net/viewtopic.php?f=23&t=13567&start=8925


The Green flags...

1. For a person with Insulin Resistance, an ad-libitum low-carb diet results in more weight loss than an ad-libitum high-carb diet.

See How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes , for an explanation.

2. For a person with Type 1 Diabetes Mellitus (T1DM), a lowish-carb (~100g/day), highish fat diet results in minimal disturbances to blood glucose levels and minimal bolus insulin doses.

See Diabetes: which are the safest carbohydrates? , to see which foods should comprise the ~100g/day. N.B. As ~50% of dietary proteins can be converted into glucose by gluconeogenesis, ~100g/day of slow-digesting proteins such as meats, eggs & cheeses can contribute ~50g/day of glucose towards the ~100g/day total.

3. For a person with LADA or MODY, see 2.

4. For a person with Type 2 Diabetes Mellitus (T2DM), a LCLF 600kcal/day Protein Sparing Modified Fast can normalise BG in 1 week and reverse T2DM in 8 weeks (provided there are sufficient surviving pancreatic beta-cells).

See http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3168743/
"After 1 week of restricted energy intake, fasting plasma glucose normalised in the diabetic group (from 9.2 ± 0.4 to 5.9 ± 0.4 mmol/l; p = 0.003)."

"Maximal insulin response became supranormal at 8 weeks (1.37 ± 0.27 vs controls 1.15 ± 0.18 nmol min−1 m−2)."

After 8 weeks, transition to a diet based on whole, minimally-refined animal & vegetable produce.

See also http://www.fend-lectures.org/index.php?menu=view&id=94

As Insulin Resistance is multi-factorial, ALL of the potential causes need to be addressed. Once this has been done, IR should be reversed, allowing restrictions on dietary carbohydrate intake to be lifted. See also Can supplements & exercise cure Type 2 diabetes?

The Red flags...

The low-carb diet is a temporary patch to ameliorate IR/IGT/Met Syn/T2DM, a bit like replacing a failed circuit-breaker by sticking a nail in its place, to allow the house to function while you fix the problem by buying a new circuit-breaker. Although the house functions fine with a nail in place of a circuit-breaker, you wouldn't want to spend the rest of your life without a working circuit-breaker protecting the house.

So, why do low-carbers seem to want to spend the rest of their lives using a temporary patch to ameliorate their IR/IGT/Met Syn/T2DM?

Long-term use of very-low-carb, very-high-fat diets is not recommended.

1. Cortisol level can gradually increase, resulting in increasing fasting BG level. See How eating sugar & starch can lower your insulin needs.

2. If you do too much high-intensity exercise, you may momentarily black-out, fall and hurt yourself. See "Funny turns": What they aren't and what they might be.

3. Some people seem to gradually go bat-shit crazy. See Can very-low-carb diets impair your mental faculties? Read the comments in https://www.facebook.com/TheFatEmperor/posts/1633434020253792. Do the behaviours of Ivor Cummins & Gearóid Ó Laoi seem normal to you?

4. Insulin Resistance is bad, mmm-kay? See Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe?

5. Dyseverything elseaemia isn't addressed. See Type 2 diabetes: between a rock and a hard place , Type 2 diabetes: your good signalling's gonna go bad and When the only tool in the box is a hammer.

6. Dietary deficiencies may develop. See Rigid diets & taking loadsa supplements to compensate for them.

7. High-fat diets with no energy deficit result in high postprandial TG's. Postprandial lipaemia is atherogenic. See Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

There may be more but I'm knackered, so I'm Publishing!

12 Eylül 2014 Cuma

Neovascularization/Neovascularisation: It doesn't ONLY cause CHD.

Another serendipitous moment.
From http://www.aao.org/theeyeshaveit/optic-fundus/retinal-neovascularization.cfm
After talking to someone with Age-related Macular Degeneration (AMD), I Googled the condition and spotted the word neovascularisation. This reminded me of Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis.

So I did a search on PubMed for Neovascularization/Neovascularisation. This is what I got:-
http://www.ncbi.nlm.nih.gov/pubmed/?term=%28%28%22neovascularization,%20pathologic%22[MeSH%20Terms]%20OR%20%28%22neovascularization%22[All%20Fields]%20AND%20%22pathologic%22[All%20Fields]%29%20OR%20%22pathologic%20neovascularization%22[All%20Fields]%20OR%20%22neovascularization%22[All%20Fields]%29%20OR%20%28%22neovascularization,%20pathologic%22[MeSH%20Terms]%20OR%20%28%22neovascularization%22[All%20Fields]%20AND%20%22pathologic%22[All%20Fields]%29%20OR%20%22pathologic%20neovascularization%22[All%20Fields]%20OR%20%22neovascularisation%22[All%20Fields]%29%29%20AND%20%28%28hasabstract[text]%20AND%20%22loattrfree%20full%20text%22[sb]%29%20AND%20%222009/09/14%22[PDAT]%20:%20%222014/09/12%22[PDAT]%20AND%20%22humans%22[MeSH%20Terms]%29%20AND%20%28hasabstract[text]%20AND%20%22loattrfree%20full%20text%22[sb]%29%20AND%20%222009/09/14%22[PDAT]%20:%20%222014/09/12%22[PDAT]%20AND%20%22humans%22[MeSH%20Terms]%20AND%20%28%28hasabstract[text]%20AND%20%22loattrfree%20full%20text%22[sb]%29%20AND%20%222009/09/14%22[PDAT]%20:%20%222014/09/12%22[PDAT]%20AND%20%22humans%22[MeSH%20Terms]%29%20AND%20%28%28hasabstract[text]%20AND%20%22loattrfree%20full%20text%22[sb]%29%20AND%20%222009/09/14%22[PDAT]%20:%20%222014/09/12%22[PDAT]%20AND%20%22humans%22[MeSH%20Terms]%29%20AND%20%28%28hasabstract[text]%20AND%20%22loattrfree%20full%20text%22[sb]%29%20AND%20%222009/09/14%22[PDat]%20:%20%222014/09/12%22[PDat]%20AND%20%22humans%22[MeSH%20Terms]%29

Even after restricting results, there were 5253 results. Wow!

It would appear that AMD has a lot in common with CHD. Ischaemia/Ischemia (lack of oxygen) to tissues causes the body to produce an adaptive response by growing new blood vessels (neovascularization/neovascularisation). Unfortunately, the new blood vessels are a bit crap, and cause other problems to develop e.g. CHD & AMD.

Therefore, prevention is better than cure. The things that lower the RR for CHD may also lower the RR for AMD. See Cholesterol And Coronary Heart Disease.

22 Ağustos 2014 Cuma

I never expected THAT to happen!

Hat-tip to Melissa McEwen for https://twitter.com/melissamcewen/status/502553259224338432


As I clicked on the video, I was thinking "I bet those instant Ramen noodles disintegrate instantly, causing a big surge of glucose into the blood".

Watch and learn. Well, did you expect that to happen? If instant Ramen noodles are a heart health risk, it's not because they digest too quickly. BPA? Something else?

8 Ağustos 2014 Cuma

Ketogenic Diets and Sudden Cardiac Death.

Last night, thanks to comments on my previous post, I stumbled across The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism, then a Google search led me to Sudden Cardiac Death and Free Fatty Acids.

The following graph is Figure 1 from Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet.
Nice Insulin, shame about the FFAs.

From the first link above:-
"Current ketogenic diets are all characterized by elevations of free fatty acids, which may lead to metabolic inefficiency by activation of the PPAR system and its associated uncoupling mitochondrial uncoupling proteins."

From the third link above:-
"Weight loss was similar between diets, but only the high-fat diet increased LDL-cholesterol concentrations. This effect was related to the lack of suppression of both fasting and 24-h FFAs."

See also Elevated plasma free fatty acids predict sudden cardiac death: a 6.85-year follow-up of 3315 patients after coronary angiography, and Circulating Nonesterified Fatty Acid Level as a Predictive Risk Factor for Sudden Death in the Population.

I think that's quite enough bad news for a Friday afternoon.


EDIT: So much for fat being a "clean-burning" fuel for the heart. Some people believe that, because dietary fats pass from the small intestine, via the Lacteals, to circulation at the Subclavian vein, this means that the heart prefers to burn fatty acids.

From Page 10 of HIGH CARBOHYDRATE DIETS: MALIGNED AND MISUNDERSTOOD:-


Did you know that Human erythrocytes (red blood cells) are loaded with cholesterol and that it can contribute towards atherosclerosis? See https://twitter.com/Drlipid/status/496625195738619904.

See also Evidence for a cholesteryl ester donor activity of LDL particles during alimentary lipemia in normolipidemic subjects. This is more evidence that very high fat meals are atherogenic, which is relevant to Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

7 Ağustos 2014 Perşembe

Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.

Like Siri-Tarino et al, Forests & Trees and "Eureka!" moments, Chowdhury et al is a meta-analysis of many studies. See Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis. I don't have access to the full study, but Google Image Search found Figure 2.
From http://annals.org/data/Journals/AIM/929862/6ff2_Figure_2_RRs_for_coronary_outcomes_in_prospective_cohort_studies_of_circulating_fatty_acid.jpeg

All saturated fatty acids have a RR for CHD of 1.06 (95% CI 0.86 - 1.30).
∴ There's no association between saturated fat intake and the RR for CHD.

Before VLC'ers do a dance of joy, consider the Forest plot for individual saturated fatty acids.
Palmitic acid has a RR for CHD of 1.15 (95% CI 0.96 - 1.37).
Stearic acid has a RR for CHD of 1.23 (95% CI 0.93 - 1.61).

Red meat & saturated fats synthesised by DNL aren't looking too good. However...
Pentadecanoic acid has a RR for CHD of 0.94 (95% CI 0.67 - 1.32).
Margaric acid has a RR for CHD of 0.77 (95% CI 0.63 - 0.93).
Pentadecanoic acid and Margaric acid combined have a RR for CHD of 0.81 (95% CI 0.62 - 1.06).

What are Pentadecanoic acid & Margaric acid found in? The clue's in the title:-
Say cheese: saturated fat in dairy may protect against diabetes.

The article in the Telegraph is actually referring to Differences in the prospective association between individual plasma phospholipid saturated fatty acids and incident type 2 diabetes: the EPIC-InterAct case-cohort study.

Of the omega-3 fatty acids...
Eicosapentaenoic acid has a RR for CHD of 0.78 (95% CI 0.65 - 0.94).
Docosahexaenoic acid has a RR for CHD of 0.79 (95% CI 0.67 - 0.93).
Eicosapentaenoic acid and Docosahexaenoic acid combined have a RR for CHD of 0.75 (95% CI 0.62 - 0.89).

Of the omega-6 fatty acids...
Arachidonic acid has a RR for CHD of 0.83 (95% CI 0.74 - 0.92).

Of the trans-fatty acids...
Trans-oleic acid has a RR for CHD of 1.20 (95% CI 0.39 - 3.73).
Trans-linoleic acid has a RR for CHD of 1.36 (95% CI 0.83 - 2.22).

21 Temmuz 2014 Pazartesi

Ancel B. Keys' critique of "Diet and coronary thrombosis. Hypothesis and fact, by John Yudkin. The Lancet, 1957."

Ancel B. Keys has come in for a lot of flak recently over alleged "cherry-picking" of data for his 6/7 Countries studies. Here's Keys' critique:- "SUCROSE IN THE DIET AND CORONARY HEART DISEASE" of Dr. John Yudkin's "15 Countries" article.

Keys accuses Yudkin of bias, cherry-picking countries that fit his own hypothesis.

Here are some plots from Keys' 11 Countries article.
5-Year CHD cases/1,000 men vs Sucrose %E.

5-Year CHD cases/1,000 men vs Sat Fats %E.

Sucrose %E vs Sat Fats %E.

So there you have it.

25 Haziran 2014 Çarşamba

The Conflation Game.

Li-i-ife, is the name of the game, and I wanna play the game with you.....


People have been "grinding my gears" by conflating carbohydrates with sugars. All sugars are carbohydrates, but not all carbohydrates are sugars. See Carbs Carbs Carbs. to find out about the five basic different types of carbohydrates.

Krauss et al has done it again. In Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia, at the bottom of Table 1 is "carbohydrate, 50% simple and 50% complex". The carbohydrates consisted of half sugars and half starches.

The effect of such a sugary diet is as follows:-

The percentage of pattern B (small, dense) LDL particles increases significantly in proportion to the percentage of Dietary "carbohydrate". The implication of this study (also A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins ) is that high-carb, low-fat diets are atherogenic.

This is not on.

A high sugar diet is atherogenic, but carbs from new potatoes (especially if eaten cold), Basmati rice (especially if eaten cold), sweet potatoes, beans & whole fruits aren't.

19 Haziran 2014 Perşembe

Siri-Tarino et al, Forests & Trees and "Eureka!" moments.

Here's Fig. 2 from Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease:-
Risk ratios and 95% CIs for fully adjusted random-effects models examining associations between saturated fat intake in relation to coronary heart disease and stroke.

The above "Forest" plot has a subtotal RR of 1.07 (95% CI 0.96 1.19). The overall conclusion is that there's no association between saturated fat intake and the RR for CHD. Hmmm.

I looked at the data in Table 3. Of the 16 studies contributing to the CHD results, only 3 of them specify high sat fat intakes over a wide range. The results from these 3 studies are as follows:-

Pietinen et al: RR=0.93 (95% CI 0.6, 1.44).
Mann et al: RR=2.77 (95% CI 1.25, 6.13).
Boniface et al: Pooled RR = 1.37 (95% CI 1.17, 1.65).

The results from Pietinen et al are statistically-insignificant (95% CI values are way above & below 1) with an overall slight protective effect. The results from Mann et al have a RR >> 1 with both 95% CI's >1 and the results from Boniface et al have a RR >1 with both 95% CI's >1.

Other studies either have sat fat intakes varying from very low to low, or specify mean/median sat fat intakes without values for highest & lowest tertiles/quartiles/quintiles etc. Other studies have results that are statistically-insignificant.

However, there are some studies that show a slight protective effect of small amounts of sat fats. How come?

Thanks to George Henderson, I had a "Eureka!" moment. He posted a link to Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis.

Here's Fig. 1 from that study.
HRs and 95% CI's of CVD risk according to quintiles of energy-adjusted SF from different sources (n = 5209).

The Meat SF plot has a net positive slope (bad news, but the range of intake is very small), the Butter & Plant SF plots are random, but the Dairy SF plot has a net negative slope (good news). Dairy saturated fats in amounts of up to 10g/day are protective against CHD. As the Dairy sat fat intake is too small to have a significant effect on lipids, what's the mechanism? I think that it's Vitamin K2. See Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.

When you average out the results from all studies, the result is null. This is data dilution statistics.

EDIT: See also Study: Saturated Fat as Bad as Sugar!

10 Haziran 2014 Salı

Ultra-high-fat (~80%) diets: Fat storage, and a delicious analogy.

Fat storage:

Here's a plot of mean (±SEM) plasma insulin concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal.
From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

100g of glucose produces a large spike in insulin concentration and 40g of fat produces no significant spike in insulin concentration. According to Gary Taubes' insulin hypothesis of obesity, in the absence of a significant spike in insulin concentration, fat cannot be stored.

Here's a plot of mean (±SEM) plasma triacylglycerol concentrations during an oral-fat-tolerance test (OFTT) when preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal (from the previous post).
From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism
Average plasma triacylglycerol concentration over 0 to 360min is ~1.3mmol/L (~116mg/dL in US units).

Plasma triacylglycerol concentration falls to baseline between 240min and 360min. OGTT's and OFTT's are performed with the subjects at rest for the duration of the test.

Referring to It's all in a day's work (as measured in Joules) , at rest the subject is burning ~1kcal/min with ~95% of it coming from fat, making a fat-burning rate of ~0.11g/min.

At a fat-burning rate of ~0.11g/min, it would take ~360min for plasma triacylglycerol to fall to baseline if the 40g of fat from the OFTT was only being burned and not being stored. As shown above, it only takes ~120min to fall to baseline. Therefore, fat from the OFTT that isn't burned is stored in ~120min in the absence of a significant insulin spike. Q.E.D.

A delicious analogy:

Here's a plot of mean (±SEM) plasma glucose concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal (from the previous post).
From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

The OGTT (100g of glucose) produces a large spike in plasma glucose concentration which lasts for ~210min before returning to baseline. Higher plasma glucose concentrations glycate more than lower plasma glucose concentrations. Average plasma glucose concentration over 0 to 360min is higher with the OGTT than with the OFTT, therefore there is more glycation damage with the OGTT than with the OFTT. Don't regularly consume 100g or more of glucose!

Here's a plot of Mean (±SEM) plasma triacylglycerol concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal.
From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism
Average plasma triacylglycerol concentration over 0 to 360min is ~1.0mmol/L (~89mg/dL in US units).

Although the plasma triacylglycerol concentration after consuming a high-carbohydrate evening meal is slightly higher than after consuming a high-fat evening meal, the two plots above are essentially flat, indicating that none of the 100g of glucose consumed was turned into fat by de novo lipogenesis (DNL) within 6 hours.

As discussed in the previous post, higher plasma triacylglycerol concentrations are more atherogenic than lower plasma triacylglycerol concentrations. Average plasma triacylglycerol concentration over 0 to 360min is higher with the OFTT than with the OGTT, therefore there is more atherogenicity with the OFTT than with the OGTT.
Don't regularly consume 40g or more of fat!

An interesting study that involved humongous fat consumption was Response of body weight to a low carbohydrate, high fat diet in normal and obese subjects , which used up to 600g of fat/day. It's possible to lose weight on an ultra-high-fat diet, but average plasma triacylglycerol concentrations would have been extremely high. Fasting TG's reduce on an ultra-high-fat diet, probably due to suppression of endogenous TG synthesis by exogenous TG intake.

Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

The good:

Here's a plot of mean (±SEM) plasma glucose concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal.
From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

An OGTT (100g of glucose dissolved in water) causes a large disturbance in blood glucose level for up to 2 hours. Ditto for insulin (see Fig. 2).

An OFTT (40g of fat as cream) doesn't cause a significant disturbance in blood glucose level. Ditto for blood insulin (see Fig. 2).

The bad:

Here's a plot of mean (±SEM) plasma triacylglycerol concentrations during an oral-fat-tolerance test (OFTT) when preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal.
From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

An OFTT (40g of fat as cream) causes a significant rise in blood triacylglycerol (a.k.a. TAG a.k.a. triglycerides a.k.a. TG's) level for up to 4 hours. Note that the effect of a preceding high-carbohydrate meal on fasting TG's is only +0.1mmol/L. Is high postprandial TG's a problem? Definitely, maybe. From Cholesterol And Coronary Heart Disease , "Cholesterol-depleted particles oxidise faster than large, cholesterol-rich ones." Chylomicrons, chylomicron remnants & VLDL-C are triglyceride-rich, cholesterol-poor, as that's the composition of the fat in the diet.

The ugly:

Here's evidence that excessive postprandial TG's significantly raise the relative risk (RR) for CHD:- See Fig. 1 in Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women.

Here's more evidence that postprandial saturated fatty TG's raise the RR for CHD:- See Postprandial triglyceride-rich lipoproteins promote invasion of human coronary artery smooth muscle cells in a fatty-acid manner through PI3k-Rac1-JNK signaling.

See also Postprandial triglyceride-rich lipoprotein changes in elderly and young subjects.,
Effect of a single high-fat meal on endothelial function in healthy subjects.,
Postprandial lipemia: emerging evidence for atherogenicity of remnant lipoproteins.,
Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men.,
Evidence for a cholesteryl ester donor activity of LDL particles during alimentary lipemia in normolipidemic subjects.,
Association of postprandial hypertriglyceridemia and carotid intima-media thickness in patients with type 2 diabetes.,
Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress.,
High-energy diets, fatty acids and endothelial cell function: implications for atherosclerosis.,
Impact of postprandial hypertriglyceridemia on vascular responses in patients with coronary artery disease: effects of ACE inhibitors and fibrates.,
[Influence of postprandial hypertriglyceridemia on the endothelial function in elderly patients with coronary heart disease].,
Impact of postprandial variation in triglyceridemia on low-density lipoprotein particle size.,
Association between fasting and postprandial triglyceride levels and carotid intima-media thickness in type 2 diabetes patients.,
[Correlation of lipemia level after fat loading with manifestation of atherosclerosis in coronary arteries].,
Postprandial hypertriglyceridemia and carotid intima-media thickness in north Indian type 2 diabetic subjects.,
Association between postprandial remnant-like particle triglyceride (RLP-TG) levels and carotid intima-media thickness (IMT) in Japanese patients with type 2 diabetes: assessment by meal tolerance tests (MTT).,
Postprandial lipemia and remnant lipoproteins.
Elevated levels of platelet microparticles in carotid atherosclerosis and during the postprandial state.,
Postprandial metabolic and hormonal responses of obese dyslipidemic subjects with metabolic syndrome to test meals, rich in carbohydrate, fat or protein.,
Atherosclerosis, diabetes and lipoproteins.
Clinical relevance of non-fasting and postprandial hypertriglyceridemia and remnant cholesterol.,
Post-prandial hypertriglyceridemia in patients with type 2 diabetes mellitus with and without macrovascular disease.,
A hypertriglyceridemic state increases high sensitivity C-reactive protein of Japanese men with normal glucose tolerance.,
CD36 inhibitors reduce postprandial hypertriglyceridemia and protect against diabetic dyslipidemia and atherosclerosis.
[Trends of evaluation of hypertriglyceridemia -from fasting to postprandial hypertriglyceridemia-].,
The effects of dietary fatty acids on the postprandial triglyceride-rich lipoprotein/apoB48 receptor axis in human monocyte/macrophage cells.

See also What Is the Significance of Postprandial Triglycerides Compared With Fasting Triglycerides? , Uncovering a Hidden Source of Cardiovascular Disease Risk and Postprandial Lipoproteins: The storm after the quiet!

A counter-argument is that the subjects in the above studies were eating carbohydrate, and that postprandial TG's aren't atherogenic if you're not eating much carbohydrate. Definitely, maybe. In the absence of carbohydrate, there is still glucose in the blood, thanks to the liver. Also, some carbohydrates don't spike blood glucose (or fructose) level. It's pure speculation that the subjects in the above studies had high blood glucose at the same time as high postprandial TG's. As Insulin Resistance/Metabolic Syndrome and/or a high-sugar diet raise fasting TG's, and there was no significant association between fasting TG's and the risk factor for CHD, this suggests that the subjects had no significant metabolic derangement and were not eating excessive amounts of sugar.

According to Very Low-Carbohydrate and Low-Fat Diets Affect Fasting Lipids and Postprandial Lipemia Differently in Overweight Men, there's a ~50% reduction in postprandial TG's after adaptation to a very-low-carb, very-high-fat diet. However, mean energy intake was only 1,850kcals/day. The subjects were in a 500kcal/day energy deficit and the %E from fat was only 60%.

Also, some people's LDL levels go extremely high on a very-low-carb, very-high-fat diet. See Lipidaholics Anonymous Case 291 Can losing weight worsen lipids? A very high LDL level results in a high LDL particle count, even if the particles are large (Type A). A high LDL particle count is a strong risk factor for CHD. See also Fig. 1 in Some Metabolic Changes Induced by Low Carbohydrate Diets.

It's possible to get Coronary Artery Calcium (CAC) scans, to measure the amount of calcified plaque in coronary arteries. While a high CAC value means lots of plaque, a zero CAC value doesn't necessarily mean zero plaque, as young people and people with a high Vitamin K2 intake don't have significant calcification. See Stenosis Can Still Exist in Absence of Coronary Calcium.

Update 26th July 2014: See Page 10 of  HIGH CARBOHYDRATE DIETS: MALIGNED AND MISUNDERSTOOD - Nathan Pritikin. Read the text, starting with:-
"Could such a cream meal precipitate an angina attack because the oxygen-carrying capacity of the blood is lowered?"
The answer appears to be "Yes."

1 Eylül 2013 Pazar

Lipoproteins & apolipoproteins: E, by 'eck.

In December 2008, I wrote about Cholesterol And Coronary Heart Disease , where I used a limousine metaphor to describe how cholesterol & fat are transported around the body. Here's a diagram of a chylomicron lipoprotein "limousine". Chylomicrons transport dietary fat (triglycerides) & cholesterol from the gut to the liver & other tissues. As there's much more dietary fat than dietary cholesterol, the contents are mostly fat.
A chylomicron. T=Triglyceride C=Cholesterol. From http://en.wikipedia.org/wiki/Lipoprotein

The lipoprotein "limousines" vary a lot in size.
(a) VLDL (b) chylomicrons (c) LDL (d) HDL. 
From http://healthcorrelator.blogspot.co.uk/2011/11/triglycerides-vldl-and-industrial.html

Apolipoproteins are the "chauffeurs" which determine to where lipoproteins transport stuff.
Apo A is found mainly on HDL, which transports fat & cholesterol from tissues to the liver.
Apo B is found mainly on LDL, which transports cholesterol from the liver to tissues.
Apo C is found on HDL when fasted, but moves to chylomicrons & VLDL when fat is eaten.
Apo D is found mainly on HDL and is is associated with an enzyme involved in lipoprotein metabolism.
Apo E is found mainly on chylomicrons & IDL and transports lipoproteins, fat-soluble vitamins, and cholesterol into the lymph system and into the blood. In the CNS, Apo E transports cholesterol to neurons. Defects in Apo E result in hyperlipidaemia , cardiovascular & neurological diseases, and is the E referred to in the title.

There's also Apo H, which is a β-glycoprotein involved in the binding of cardiolipin. It has nothing to do with the above lipoproteins.

19 Haziran 2013 Çarşamba

Completing the trine: Which are the safest fats?

First, watch this video by Chris Masterjohn.

Diets very high in pufas (polyunsaturates) are not beneficial to heart health or longevity. Flora? No thanks!

Here's a chart. The beige & grey bars represent pufas (omega-6 & omega-3).
Comparison of dietary fats
The yellow bars represent monounsaturates and the orangey-red bars represent saturates. I consider these to be harmless, as long as you don't go mad and eat them in such large amounts that you gain weight.

Bearing in mind the information in the video, plus the information in Fats: Spawn of Satan or Dogs' Doodads? , I use only fats from the bottom 6 for cooking (olive oil and butter, actually).

Flaxseed oil can be used as an omega-3 supplement for vegetarian/vegan women, as omega-3 pufas are as rare as rocking-horse poo in most foods (apart from oily fish).

Non-vegetarian/vegan people can get their long-chain omega-3 pufas (EPA & DHA) from oily fish. As vegetarian/vegan men barely produce any DHA from the omega-3 in flaxseed oil, they should get it from algal DHA supplements. See Extremely Limited Synthesis of Long Chain Polyunsaturates in Adults: Implications for their Dietary Essentiality and use as Supplements.

30 Mayıs 2013 Perşembe

The danger of science denial: It happens even on Science-Based blogs.

Poor Benjamin Franklin. I know how he felt! ;-)
I do not believe that he wanted to be doing that!
This post will be highly critical of Dr. David Gorski MD, as some of his comments have been either trolling, downright stupid, or both. They're definitely in denial of science. This post is intended to encourage Dr Gorski to leave comments here, as I will never leave any further comments on any blogs that he edits, for reasons mentioned previously. I will be copying comments from his blogs and pasting them here, with my comments after. If this is considered to be "bad form", I really don't care. Leaving derogatory comments about me on blogs on which the commenters know that I will never return (because I told them so) is definitely "bad form".

I will also be quoting other commenters on Dr Gorski's blog, for the same reason. Everyone is free to leave comments here, that meet my fairly lax moderation criteria. In Vitamin D, cancer, cliques and flouncing. , a commenter from Dr Gorski's blog called flip was initially whitelisted, to allow his comments to appear without me having to moderate them. I eventually blacklisted flip after I detected intellectual dishonesty. That's how I roll. If you don't like my rules, don't let the door hit you on the way out! By the way, calling me a liar on here is a sure-fire way to get yourself blacklisted.

I've just turned Blogger word verification back on, as although Disqus automatically deletes anonymous comments containing links, I still get email notification of them. I've been getting a lot of email notifications. This may or may not have an effect on commenters.

Firstly, please read http://www.sciencebasedmedicine.org/index.php/a-closer-look-at-vitamin-injections/#comment-127850 , as it's my "letter of resignation" from that blog. With that in mind, read on.

# David Gorski on 27 May 2013 at 9:49 am
Regarding Lappe et al, one notes that that study is not the be-all and end-all of vitamin D research. It’s an old study, for one thing. Also, cancer was not its primary endpoint. Finally, there was no vitamin D alone group, as I recall, only a vitamin D + calcium group, a calcium group, and a placebo group.
There is a recent review of the literature from the Endocrine Society, which includes Lappe et al and puts it into context:
*quoted text redacted*

# Nigel Kinbrum on 27 May 2013 at 11:16 am
David Gorski said…
Regarding Lappe et al, one notes that that study is not the be-all and end-all of vitamin D research. It’s an old study, for one thing.
Irrelevant.
Also, cancer was not its primary endpoint.
Irrelevant.
Finally, there was no vitamin D alone group, as I recall, only a vitamin D + calcium group, a calcium group, and a placebo group.
Irrelevant.

# David Gorski on 27 May 2013 at 12:28 pm
Finally, there was no vitamin D alone group, as I recall, only a vitamin D + calcium group, a calcium group, and a placebo group.
Irrelevant.
How so? It’s actually very, very relevant, as is the issue of cancer not being a primary outcome measure of the study. That you don’t understand why these issues are so relevant indicates to me that you don’t understand clinical research very well.

#Nigel Kinbrumon 27 May 2013 at 1:42 pm
David Gorski said…
Finally, there was no vitamin D alone group, as I recall, only a vitamin D + calcium group, a calcium group, and a placebo group.
Irrelevant.
How so? It’s actually very, very relevant, as is the issue of cancer not being a primary outcome measure of the study. That you don’t understand why these issues are so relevant indicates to me that you don’t understand clinical research very well.
1) The RCT used Ca + D. Therefore, the conclusions apply to Ca + D. If they’d wanted to test D alone, they would have. They didn’t. Why don’t you write a letter of complaint to Joan M Lappe about it?

2) Whether the outcome was primary, secondary, tertiary, quaternary or n’ary is irrelevant because the parameter in question (all-cancer diagnoses) was still accurately recorded. That you can’t understand such a simple concept boggles my imagination.

#David Gorski on 27 May 2013 at 2:34 pm
As I’m leaving permanently, what’s the point?
Ah, flouncing off again. It’s probably long overdue. I’ve been getting a few complaints about you here as well. Perhaps you should ask yourself why complaints seem to follow you wherever you go.
“Whether the outcome was primary, secondary, tertiary, quaternary or n’ary is irrelevant because the parameter in question (all-cancer diagnoses) was still accurately recorded. That you can’t understand such a simple concept boggles my imagination.”
I rest my case that you do not understand clinical trial methodology and interpretation. I couldn’t have demonstrated it better myself to anyone who actually does understand clinical trial methodology and interpretation. Thanks!

You sir, are an asshole. I spelled it the American way, just for you!

I rest my case that you're either trolling, or stupid, or both. Whether the outcome is primary, secondary, tertiary, quaternary or n’ary is completely and utterly irrelevant. It always has been and it always will be. You're effectively saying that only the first item in a shopping list should be bought because all of the other items in the shopping list are irrelevant. Bullshit!

Denice Walter May 27, 2013
@ Marc Stevens Is Insane:
I believe that Nigel is like two bright guys I know: they are well educated and professional in fields outside of SBM/ life sciences (business). Thus they read alt med ‘research’ (also see today’s post by Orac) and don’t get how it DOESN’T work in reality. It sounds like nutrients can do all of these wonderful things – that they can’t- at least not in RL. But the woo-meisters don’t tell you that part. We do.

So of course they think that these products are very useful- and they need celtic salt or ground organic flaxseed- as I know all too well.

However, if they’re smart- we can talk to them:
explaining how that *in vitro/ in vivo* thing works.
Or- as I often do- illustrating how much of the so-called science they read ( woo) is actually more accurately called “advertising copy”.

Businessmen seem to grok that.

Denice, seriously? I'm disappointed. I thought that you were one of the few reasonable posters on Gorski's blog and then you go and write that crap?

I do not read "alt med ‘research’", unless you're calling what's on PubMed "alt med ‘research’"? I've been reading studies on PubMed for years, so I know about the use of shoddy methodology to fudge results. The Lappe study doesn't use shoddy methodology. It's a Randomised Controlled Trial using double-blinded placebos and randomly-selected subjects who were post-menopausal women. Try to pick holes in it.

flip May 29, 2013
Hmmm… it occurs to me I probably haven’t been that overt about one other thing:

Lilady, I am sorry that you were called those things, and I certainly don’t think you should have been called names. I do think Nigel was wrong and do think he should be called out for it.

And I’m sorry for not making that clearer before.

flip, I'm not going to question your intelligence. However, why you're apologising to lilady boggles the imagination. lilady is a despicable human being. She pushed me to the point where I called her rude names, names that were not misogynist and for which I apologised. I explained about "twat" on SBM. I even posted a link to Wiktionary! You don't read things thoroughly before commenting.

Marc Stephens Is Insane May 31, 2013
Oooooh, Nigeepoo is ANGRY! He’s pulled a DJT, posting a “rebuttal” to all the comments here and on SBM. I’m suprised it’s taken him this long.

He’s calling Orac an a**hole and stupid, among other things. He’s invited us all to comment on his blog because he has an “open moderation policy” and “allows all comments.”

http://nigeepoo.blogspot.com.au/

I see that you idiots on RI are still reading my blog. I'm not the slightest bit angry, so you can give the projection crap a rest. For the record, most of you come across as assholes. You can't even quote me correctly. I said that I have fairly lax moderation criteria. Do try to get something right, for once in your miserable lives.

Anyway, you lot are now boring me with your never-ending inability to discuss things either accurately or rationally, so I'm not going to bother polluting my blog with any more of your crap.

P.S. I still occasionally read the comments on Gorski's blogs, so for the benefit of you peeps who read mine:-
1) "Black-list" means exactly what it says. It means that you're banned from posting comments.
2) The Lappe et al 2007 study was a good study. Just because some Messiah-like person says that it's a bad study and applies false reasoning to back himself up, doesn't make him right and me wrong. As I've previously pointed out, surgery's not exactly rocket science is it? I designed complicated electronic communications systems for 29 years. Just saying! ;-) Denice, I've got nothing against you. You've just been drinking Gorski's Kool-Aid for way too long. That's not a euphemism, by the way! :-D

Look what I just found. Exposing Dr. David H. Gorski, M.D., Ph.D. who believes he can use a cloak of anonymity and character assaults to discredit opposing views. Sorry Doc, but your game is up.

He's not the Messiah. He's a very naughty boy! :-D

28 Mayıs 2013 Salı

\ curves and U curves: Vitamins D3 and K2 again.

Here are some curves relating to Vitamin D. Ref: http://www.ncbi.nlm.nih.gov/pubmed/23601272
Hazard Ratios (HRs) vs serum Vitamin D level
The solid lines are the 95% confidence intervals (CI) & mean for all-cause mortality. 95% CI's are the values within which 95% of the subjects tested fall. 2.5% fall below the lower CI and 2.5% fall above the upper CI. The dashed lines are the 95% CIs & mean for coronary heart disease (CHD) mortality. Most of the curves follow a \ curve, indicating that more Vitamin D is better, up to 66ng/mL (150nmol/L, the level that I'm at). The interesting curve is the upper dashed line, which follows a U curve.

The U curve indicates that a Vitamin D level of greater than 30ng/mL (75nmol/L) increases the Hazard Ratio (HR) for CHD in the top 2.5% of subjects only, relative to 30ng/mL, even though the mean HRs for CHD & all-cause mortality (the more important parameter) are decreasing, up to 66ng/mL. What's occurring?

See Vitamin K. The increase in HR for CHD mortality above 30ng/mL in the top 2.5% of subjects only is almost certainly due to calcification within artery walls, due to under-carboxylation of osteocalcin in bone Matrix Gla Proteins, caused by insufficient Vitamin K2 rather than excessive Vitamin D. This is why I supplement with Vitamin K2. See also Vitamin D toxicity redefined: vitamin K and the molecular mechanism.

19 Mayıs 2013 Pazar

Vitamin D, cancer, cliques and flouncing.

First Google Image Search result for Vitamin D, cancer, cliques and flouncing.
This is a continuation of my previous post Enzyme kinetics, standing on the sun and weird blog comments sections.

Apparently, I didn't like the answers that I received on the blog in my previous post, so I flounced. The study that I asked for opinion on was Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. If I showed you an RCT where deaths from all cancers fell by 77%, what would be your reaction? My reaction would be "That looks promising. More work is needed to investigate it". One person (sophia8) reacted thusly. Other reactions that I received (with their logical fallacies) were as follows:-

Pure coincidence. Argumentum ad ignorantiam.

More than 1,100iu/day of Vitamin D is harmful. Straw man. I didn't say that people should take more than 1,100iu/day of Vitamin D (even though I take 5,000iu/day, which isn't harmful). Also, argumentum ad ignorantiam. See enzyme kinetics in the previous post.

You're cranky. Ignoratio Elenchi.

The study wasn't testing Vitamin D on its own. Straw man. I didn't say that it did.

By the way, “Nigeepoo”, taking supplemental vitamin D is not a proven way to prevent sunburn and is not an adequate method of protection from getting skin cancer (despite assertions in your blog). Straw man for the first part of the sentence. I didn't say that it was. Argumentum ad ignorantiam for the last part of the sentence.

Going for long drives with the top down and broiling gently without sunscreen on a repeated basis is dumb. Straw man. I didn't say that I did. I obviously don't go for long drives with the top down in the middle of the day on a sunny Summer's day. That is dumb. Like, duh!

I'm curious why you found my response to be satisfactory but lilady’s to be unsatisfactory. Could you explain? Ignoratio Elenchi.

Did I mention all of the mis-quoting?... Oy!

Maybe they should have done a bit of basic research, like:-

Vitamin D and musculoskeletal health, cardiovascular disease, autoimmunity and cancer: Recommendations for clinical practice.

The effect of calcium and vitamin D supplementation on obesity in postmenopausal women: secondary analysis for a large-scale, placebo controlled, double-blind, 4-year longitudinal clinical trial.

Vitamin D, cardiovascular disease and mortality.

Why randomized controlled trials of calcium and vitamin D sometimes fail. Essential reading.

I'm the sort of person who's not interested in cliques or secret societies. I'm therefore not interested in joining a cliquey, ivory-towery blog where you have to conform to a set of unwritten "rules" to be accepted, some of which are eccentric (Question: Which blogs insist on the use of manually-typed blockquote tags? Answer: Only that one). I decided to leave. I even apologised to some commenters for my language in some of the arguments.

I wondered why that blog and its owner annoyed me so much. Then it hit me (like a discarded boomerang)!
 
Hmmm. See Brain Surgeon meets Rocket Scientist ;-)

Other comments:-

Orac
May 19, 2013
Nigel, you need to tone it down, too.
I’ve warned both of you once already. This is the second warning. There won’t be a third. To show you I mean business this time, your comments are going into automatic moderation. You two have already wasted more of my time than you’re worth.

Which part of "Can people please stop leaving comments aimed at me, unless it’s an acknowledgement. I don’t want to have to leave any more comments on here – ever." did you not understand?

MI Dawn
May 19, 2013
@Nigel: we responded to the Lappe information. It didn’t prove what you say it proved. Now, if you do have something to say, give the peer-reviewed proof.

Straw man. I didn't say that it proved anything.
Which part of "Can people please stop leaving comments aimed at me, unless it’s an acknowledgement. I don’t want to have to leave any more comments on here – ever." did you not understand?

lilady
May 19, 2013
Thank you Orac for your intervention.
The bottom line for Nigel and Lisa is that they, by their vicious unwarranted personal attacks, have drawn unfavorable publicity to themselves and their blogs.

There's no such thing as unfavorable (sic) publicity for my blog, as far as I'm concerned. What you have done, by your vicious, unwarranted, lying and malicious defamatory personal attacks on me, is to draw unfavourable interest from me.

flip
In a place where no federal police turned up today
May 20, 2013
What a pity they both seem to have flounced off without bothering to respond to the questions put to them. I am not surprised though.

Which part of "Can people please stop leaving comments aimed at me, unless it’s an acknowledgement. I don’t want to have to leave any more comments on here – ever." did you not understand?