Re: Diet sugars and cardiovascular disease

[Guest guest]

Hi folks:

I didn't read all of Al's post below. But from what I did read, it

seems to have a message that tends to confirm the suspicions of some

people here regarding what may be the best way to implement 'CR'.

After doing as Francesca advises for implementing 'ON' : " first stop

eating the junk " , (someone should put that in the Dictionary of

Quotations!!!) and therefore having arrived at a diet composed of

healthy foods, but perhaps with a not-much-reduced caloric intake,

how should one then proceed to reduce the calories?

The answer that seems to drop neatly out of the material in Al's post

is: gradually reduce intake of starch. Not to zero, but enough to

get caloric intake down to where one would like it to be. There are

a number of reasons for this approach.

First, its high glycemic index which, more and more it seems,

especially in Al's post, does matter, at least to some extent.

Second, there is no nutritional need for starch beyond its provision

of calories. These calories were very important to many of our

ancestors at a time when food deprivation, at least on a seasonal

basis, was the norm. But it does not seem likely that caloric

deprivation will ever be important to us except in the case of a

major asteroid strike.

Third, there are some lingering suggestions of a modest starch/cancer

connection, perhaps due to aflatoxin contamination in the growing,

processing or storage of the product. Or, possibly, because those

eating a lot of starch may not be consuming enough 'micronutrient

dense', i.e. cancer protective, foods.

For those who believe that whole grain products are just wonderful

(perhaps they truly are?) as well as for those who believe one should

not eliminate a whole food group entirely, one can add bran and germ

to the diet in an amount equivalent to what is lost by foregoing the

whole grain. If whole grain products truly are as beneficial as many

believe, it must be, after all, the bran and germ that are the reason

for the benefit.

Anyway, reducing the starch is the way I am doing it. And after a

lifetime of eating, and enjoying, considerable quantities of bread

and potatoes that is a considerable sacrifice.

All just one person's opinion. (Subject to change without notice!).

Rodney.

--- In , " old542000 " <apater@m...>

wrote:

>

> Hi All,

>

> I thought although CR receives only some

> rather passing attention in the below, the issue

> of the glycemic index of our food and the glycemia

> that we may consequently suffer play a larger role

> for us.

>

> A good introduction to the topic may be:

>

> http://lists.calorierestriction.org/cgi-bin/wa?

>

A2=ind0411 & L=crsociety & P=R1549 & D=0 & X=5F1CA53A791170A5E5 & Y=old542000@ya

> hoo.com

>

> http://tinyurl.com/4auja

>

> The papers in the post above refers to reference 51

> in the below pdf excerpts and are in http://tinyurl.com/4fxzj

>

> for:

>

> Ann Intern Med. 2004 Nov 2;141(9):738; author reply 738-9.

>

> Overall, lower carbohydrates diets are preferred among

> us for CR. I would tend to, reluctantly, agree. It goes

> against my palate and thrifty disposition.

>

> Dickinson S, Brand- J.

> Glycemic index, postprandial glycemia and cardiovascular disease.

> Curr Opin Lipidol. 2005 Feb;16(1):69-75.

> PMID: 15650566 [PubMed - in process]

>

> Purpose of review: Several lines of evidence indicate that

> exaggerated postprandial glycemia puts individuals without diabetes

> at greater risk of developing cardiovascular disease. In large,

> prospective observational studies, including metaanalyses, higher

120

> min post-load blood glucose and glycated hemoglobin (a measure of

> average blood glucose level over time) independently predict

> cardiovascular mortality and morbidity in individuals without

> diabetes. These findings imply that the glycemic nature of dietary

> carbohydrates may also be relevant. We aim to provide a clearer

> perspective on how the glycemic impact of carbohydrates may

modulate

> development of cardiovascular disease.

> Recent findings: In ecological studies, average dietary glycemic

> index (a measure of the postprandial glycemic potential of

> carbohydrates) and glycemic load (average glycemic index × amount

of

> carbohydrate) predicts coronary infarct and cardiovascular disease

> risk factors, including HDL cholesterol, triglycerides and C-

reactive

> protein. In short-term intervention studies of overweight and

> hyperlipidemic patients, low glycemic index diets lead to

> improvements in cardiovascular disease risk factors, including

> reduced LDL cholesterol and improved insulin sensitivity, as well

as

> greater body fat loss on energy-restricted diets. Molecular studies

> indicate that physiological hyperglycemia induces overproduction of

> superoxide by the mitochondrial electron-transport chain, resulting

> in inflammatory responses and endothelial dysfunction.

> Summary: Taken together, the findings suggest that conventional

> high-carbohydrate diets with their high glycemic index may be

> suboptimal, particularly in insulin-resistant individuals. Because

> around one in four adults has impairments in postprandial glucose

> regulation, the glycemic potential of carbohydrates warrants

further

> investigation in cardiovascular disease prevention.

>

> Abbreviations BMI: body mass index; CRP: C-reactive protein;

CVD:

> cardiovascular disease; HbA1c: hemoglobin A1c; HOMA: homeostasis

> model assessment; IGT: impaired glucose tolerance; PPG postprandial

> glycem.

>

> Introduction

> Over the past decade, dietary advice to reduce the risk of

> cardiovascular disease (CVD) and obesity has recommended

> carbohydrates in place of saturated fatty acids, with little

emphasis

> on the nature of the carbohydrate. There is concern, however, that

> some high-carbohydrate diets may increase the risk of CVD, type 2

> diabetes and obesity, especially those that exaggerate postprandial

> glycemic and insulin responses and dyslipidemia [1•,2•]. In this

> context, the use of the glycemic index approach to classifying

> carbohydrates has provided insights that the traditional separation

> of carbohydrates into starch and sugars has not [3]. The glycemic

> index compares carbohydrates gram for gram in individual foods,

> providing a numerical, evidence-based index of postprandial

glycemia

> [4]. A lower glycemic index suggests a slower rate of digestion and

> absorption of the sugars and starches in foods but may also

indicate

> greater hepatic and peripheral extraction of the products of

> carbohydrate digestion [5]. The glycemic index has provoked

> controversy, particularly in relation to diebetic diets but there

is

> agreement that moderate-to high carbohydrate based on low glycemic

> index foods (not low carbohydrate diets) provide a benefit to

> glycemic control [6••].

> Several lines of evidence support the hypothesis that an

excessive

> rise in blood glucose levels after a meal increases the risk of

> chronic disease. The first is that dominated by the

> term `postprandial or post-challenge glycemia' (PPG) and its

> continuous relationship to cardiovascular and total mortality in

> individuals with or without diabetes. The second area is that

denoted

> by the keywords `glycemic index' and `glycemic load' (the product

of

> the glycemic index of specific foods and the carbohydrate content

per

> serving). A third avenue of research indicates that hyperglycemia,

> even within the normal nondiabetic range, is directly involved in

> pathogenic processes because it creates oxidative stress. This

review

> aims to bring the three areas together to provide a clearer

> perspective on how the glycemic impact of carbohydrates may

modulate

> the development of CVD.

>

> Impaired glucose metabolism

> Impaired glucose metabolism is surprisingly common even in those

> without diabetes. In Australia, almost 25% of approximately 11 000

> adults surveyed in the Australian Diabetes, Obesity and Lifestyle

> study had either diabetes or impaired glucose metabolism, including

> impaired glucose tolerance (IGT) and impaired fasting glucose [7].

On

> a worldwide basis, abnormal glucose metabolism is more common in

> indigenous, South Asian, Chinese and Asian-Indian populations, with

> lower prevalence in Caucasians [8•]. IGT indicates not only the

> presence of insulin resistance but also loss of early first phase

> insulin secretion. While many individuals accommodate higher

> carbohydrate intake by increasing insulin sensitivity, others

require

> increased insulin secretion to maintain normal glucose homoeostasis

> [9]. Because [beta]-cell defects may also be present, insulin

> secretion may be compromised over the long term. A significant

> proportion of individuals will therefore display postprandial

> glycemia (PPG) as they age. The implications of this defect are

> important because every meal, particularly high-carbohydrate meals,

> represents a challenge to glucose homoeostasis. While a 75 g

glucose

> load may not be `physiological' in a strict sense, it is not

> materially different in glycemic impact to a typical meal

containing

> 50 or 75 g starch or sugars. On a scale where glucose = 100, the

> glycemic index of most modern starchy foods is above 70, including

> bread, potatoes, rice and breakfast cereals [4]. While additional

fat

> and protein in a meal reduce the glycemic response, the rank order

of

> responses to different carbohydrates in the mixed meal is still

> predicted by the glycemic index of the single foods [10•]. Low-fat,

> high-carbohydrate meals based on high glycemic index food sources

> produce the highest day-long glycemic profiles [11••].

>

> Post-challenge glycemia as a risk factor for cardiovascular

disease

> A high 2 h post-challenge blood glucose level is increasingly

> recognized as an important independent risk factor for CVD in

> individuals without diabetes. The heightened risk in people with

> diabetes is well established, beginning well before the development

> of diabetes when only moderate increases in PPG are present [12].

> Moreover, poor control of hyperglycemia plays a significant role in

> progression of CVD in people with diabetes. While large,

prospective

> clinical trials have shown a direct relationship between the degree

> of glycemia and diabetic microvascular complications, the link to

> macrovascular complications is less clear. In the UK Prospective

> Diabetes Study, for example, higher levels of glycated hemoglobin

A1c

> (HbA1c) did not predict a significantly greater risk of CVD [13].

In

> people with diabetes, however, HbA1c reflects average blood glucose

> levels rather than postprandial `spikes' and does not distinguish

> between larger and smaller fluctuations in PPG [14]. In recent

years,

> controlling PPG per se has become the focus of new therapeutic

> approaches to reduce the burden of CVD complications in people with

> diabetes.

> In prospective cohort studies, high post-challenge blood glucose

> is associated with all-cause and CVD mortality. The relative risk

is

> up to three times greater when comparing extreme quintiles or

> quartiles [15,16]. Most recently, Levitan et al. [17••] conducted a

> meta-analysis of 39 reports in nondiabetic populations of the risk

of

> CVD in relation to 120 min post-load glucose values. The group with

> the highest post-challenge blood glucose had a 27% greater risk of

> CVD than the group with the lowest glucose levels and the relative

> risk was higher in women than men (1.56 versus 1.23). Adjustment

for

> traditional CVD risk factors attenuated but did not abolish the

> relationship. Glycemic `spikes' have also been more strongly

> associated with carotid intima-media thickness than fasting glucose

> or HbA1c [18]. Hanefeld et al. [19] showed that intima-media

> thickness increased 13% comparing the lowest and highest quintiles

of

> 2 h PPG in a group of 403 European individuals without diabetes.

> nsen et al. [20••] found a strong, independent relationship

> between HbA1c in around 6000 individuals without diabetes and the

> risk of developing hard plaques. The odds ratio was 5.8 in the

> highest quintile of HbA1c and remained significant after adjustment

> for possible confounders, including body mass index (BMI),

> hypertension and physical activity. Increased risk was present even

> at modestly elevated levels of HbA1c.

>

> Glycemic index, glycemic load and cardiovascular disease risk

> Studies incorporating the glycemic index and glycemic load

provide

> the second line of evidence that excessive PPG increases the risk

of

> CVD. In this context, the glycemic index allows a more

physiological

> basis for comparing carbohydrates than the traditional starch

versus

> sugar classification. This is because there is no clear distinction

> between the size of the carbohydrate molecule or chain length and

the

> level of PPG. Indeed, many modern starchy foods produce higher

levels

> of glycemia than sugar-containing foods [4]. Dairy products, fruits

> and chocolate confectionery in particular may contain high levels

of

> simple sugars, yet have low glycemic index values (<50). At the

other

> extreme, many low-fat, high-starch foods have exceptionally high

> glycemic index values (>80), although pasta and legumes are

important

> exceptions. Moreover, dietary fiber is not a reliable predictor of

> PPG, particularly in respect of flour-based products. Most

wheatmeal

> breads and high-fiber breakfast cereals have high glycemic index

> values that are similar to their refined counterparts [4]. For this

> reason, using the glycemic index is a more precise instrument for

> teasing out the effects of PPG per se on disease risk.

> Glycemic load is defined as the product of the carbohydrate

> content per serving of food and its glycemic index. It was

introduced

> by Harvard researchers to derive a `global' estimate of

postprandial

> glycemia and insulin demand [3]. Recent studies have validated the

> concept in a physiological sense. Servings of food with the same

> glycemic load produced similar levels of postprandial glycemia, and

> step-wise increases in glycemic load gave predictable increases in

> glycemia and insulinemia [21]. Moreover, when four isoenergetic

diets

> of differing glycemic load were compared in mixed meals over 10 h,

> they produced the expected rank order of responses [10•]. Diets

based

> on large quantities of carbohydrates from high glycemic index

sources

> such as bread, potatoes and breakfast cereals therefore have the

> highest glycemic load and theoretically the highest levels of PPG.

> Liu et al. [22] were the first to consider glycemic index,

> glycemic load and CVD using data from 75 000 women in the Nurses'

> Health Study. During 10 years of follow-up, dietary glycemic load

was

> directly associated with risk of coronary heart disease after

> adjustment for known confounders, including fiber. The relative

risk

> comparing highest and lowest quintiles was 1.98 and was most

evident

> among women with a BMI above 23. In addition, infarct risk was not

> predicted by the amounts of sugar or starch in the diet.

> Two studies, one large and one small, found no strong

association

> between glycemic index and nonfatal myocardial infarction. In the

> Zutphen study of elderly men [23], for example, the relative risk

was

> only 1.11 from lowest to highest tertile of glycemic index.

> Similarly, in an Italian population of 433 men without diabetes

[24],

> glycemic index was not significantly related to disease risk,

except

> in the subgroup of men over 60 years with a BMI greater than 25.

One

> of the particular strengths of the Harvard research, however, is

the

> quality of the glycemic index database. of the

> University of Toronto, who first proposed a glycemic index of

foods,

> coded the Harvard database and tested some of the key foods.

Because

> many breads and cereal products have unknown glycemic index values,

> extrapolation may be a significant source of error and create bias

> towards the null hypothesis.

>

> Glycemic index, glycemic load and dyslipidemia

> The glycemic index and glycemic load may influence risk of CVD

via

> mechanisms other than PPG. HDL cholesterol is a powerful predictor

of

> the development of CVD. In metabolic studies, diets with increased

> carbohydrates are recognized to reduce HDL cholesterol

concentration

> and increase triglycerides [25]. But quality of the carbohydrate

may

> also be important in this regard. HDL cholesterol has been found to

> correlate with the glycemic index of the diet in different

countries

> and population groups [26–28]. In a cross-sectional study of middle-

> aged British adults, the glycemic index was the only dietary

variable

> significantly related to serum HDL cholesterol and a stronger

> predictor than dietary fat [29]. Using data from nearly 14 000

> Americans in the Third National Health and Nutrition Examination

> Survey, Ford and Liu [28] found an inverse relationship between

> glycemic index and glycemic load and HDL cholesterol across all

> subgroups of participants categorized by sex or BMI.

> Dietary glycemic load has also been directly related to fasting

> triglyceride levels. In a subgroup of 185 healthy post-menopausal

> women from the NHS, both glycemic index and carbohydrate

contributed

> independently to a strong positive association between glycemic

load

> and fasting triglycerides [27]. The relationship was steeper and

> stronger in those with a higher BMI. For the lowest and highest

> quintiles of glycemic load, the mean triglycerides were 0.92 and

2.24

> mM in the women with BMI greater than 25, and 1.02 and 1.42 in

women

> with BMI less than or equal to 25. In this same cohort, glycemic

load

> was also associated with increasing levels of C-reactive protein

> (CRP), a measure of chronic low-grade inflammation [30]. In obese

> subjects, Harbis et al. [31•] found that high glycemic index

> carbohydrates create a detrimental postprandial pattern in

> triglyceride-rich lipoproteins derived from both hepatic and

> intestinal sources. These data support the physiological relevance

of

> glycemic load, particularly in those prone to insulin resistance.

> Diets with a high glycemic index or glycemic load appear to

> influence the development of the metabolic syndrome. In the

> Framingham Offspring Study [32•], the relative risk of having the

> syndrome using the ATP1 criteria was 1.41 comparing highest and

> lowest quintiles of glycemic index, independently of dietary fiber

> intake. Total carbohydrate and glycemic load, however, were not

> associated with prevalence of the metabolic syndrome.

> Hyperinsulinemia itself, the compensatory response to PPG in the

> presence of insulin resistance, may contribute directly to the

> pathogenesis of CVD. In the Framingham offspring study, homeostasis

> model assessment (HOMA)-insulin resistance was associated with

> increasing glycemic index [32•] and similarly, in a group of

healthy

> children, fasting insulin was predicted by the glycemic index of

the

> overall diet [33•].

>

> Intervention studies using low glycemic index diets

> Several short-term clinical trials in healthy and normoglycemic,

> high-risk individuals provide direct evidence that diets with a low

> glycemic index improve hyperlipidemia and insulin sensitivity. In

> hyperlipidemic patients without diabetes, 's group

[34]

> demonstrated that 4 weeks on a low glycemic index diet could reduce

> total cholesterol and LDL cholesterol by around 10% and

triglycerides

> by around 20% in comparison with a macronutrient and fiber-matched

> high glycemic index diet. HDL levels, however, remained unchanged.

> Frost's group extended these findings in women with advanced

CVD

> awaiting bypass surgery. Glucose tolerance and insulin sensitivity

> improved after 4 weeks on a low glycemic index diet (versus the

high

> glycemic index diet) as judged by the insulin area under the curve

in

> response to a glucose challenge [35]. In overweight, middle-aged

men,

> Brynes et al. [11••] showed that postprandial HOMA-insulin

resistance

> increased significantly more on a high glycemic index diet (+31%)

> than a macronutrient-matched low glycemic index diet (-43%).

> Similarly, Patel et al. [36•] demonstrated improved glucose

tolerance

> and postprandial glycemia and insulin in men scheduled for bypass

> surgery. In this study, length of hospital stay after surgery was

> shortened significantly in the group randomized to the low glycemic

> index diet versus the high glycemic index diet (7.1 versus 9.5

days).

> Low glycemic index diets have also resulted in improved lipid

> metabolism in healthy, overweight individuals consuming high-

> carbohydrate foods ad libitum. After a 10-week energy-restricted

> intervention, Sloth et al. [37••] demonstrated no differences in

> weight loss between the high and low glycemic index groups, but

> significant decreases in LDL cholesterol on the low glycemic index

> diet. Low glycemic index diets also have improved glucose and lipid

> metabolism in patients with diabetes. A recent meta-analysis found

a

> significant reduction in total and LDL cholesterol in individuals

> with type 2 diabetes but no effect on triglycerides and HDL

> cholesterol [38••].

> Intervention studies using drugs that specifically target PPG

> provide direct evidence that elevated blood glucose levels affect

CVD

> endpoints in individuals without diabetes. In the STOP-NIDDM study,

> for example, patients with IGT who had been randomized to acarbose

> (an [alpha]-glucosidase inhibitor that slows carbohydrate

absorption)

> had half the risk of a cardiovascular event or hypertension over

the

> 3-year period compared with those given the placebo [39••].

> Furthermore, annual progression of intima-media thickness was

> significantly reduced in the acarbose-treated group by around 50%

> [40•]. This is an important study in the present context because

the

> mechanism of action can only be ascribed to the slowing of

> carbohydrate absorption and consequent reduction in PPG – a

property

> analogous to that of low glycemic index foods. Thus, while it is

> possible that low glycemic index foods improve risk by virtue of

> their wholegrain nature, fiber or micronutrient content, the

slowing

> of carbohydrate absorption per se is probably their most important

> attribute.

>

> Glycemic index and weight control

> There is increasing evidence that the glycemic index has

> implications for weight control and therefore for CVD. In

particular,

> wide fluctuations in blood glucose and insulin levels have been

> linked to appetite stimulation in human and animal studies [41]. In

> one-day studies, meals containing low glycemic index carbohydrate

> have been found to enhance satiety and reduce total energy intake

at

> the following meal [42,43]. High glycemic index meals have also

been

> associated with reduced fat oxidation at rest and during exercise

> [44,45] and lower metabolic rate during and after weight loss [46].

A

> limited number of controlled trials demonstrate faster or more

> sustained weight loss on low glycemic index diets [47–49].

> We recently completed a study in 129 young overweight volunteers

> comparing four diets of varying glycemic load (i.e. they varied in

> both glycemic index and carbohydrate content but not fat) over a 12-

> week period. Most foods were supplied but the amount eaten was at

the

> discretion of the individual. The findings indicate that body fat

> loss was enhanced on both the low glycemic index (55% energy as

> carbohydrate, 15% protein) and the lower-carbohydrate (45%

> carbohydrate, 25% protein) diet compared with the conventional low-

> fat diet. Improvements in lipid metabolism, however, were

> significantly greater in the low glycemic index group than in any

> other groups. These findings are broadly consistent with recent

> studies of very low carbohydrate diets. Reducing the glycemic load

of

> the diet by severe restriction in carbohydrate intake results in

> faster rates of weight loss in the first 6 months and improved

lipid

> profiles at 12 months, even after adjustment for differences in

> weight loss [50•, 51••]. However, because very low carbohydrate

diets

> are unavoidably high in total and saturated fat, there may be long-

> term cardiovascular implications. In contrast, there are no such

> concerns in respect of high-carbohydrate, low glycemic index diets.

> Because manipulation of a diet's glycemic index can produce

> changes in potentially confounding dietary factors, such as fiber

> content, palatability and energy density, its relevance to health

> remains controversial. In this context, long-term studies in

animals

> provide additional evidence that low glycemic index is important in

> relation to weight gain, body fat and diabetes risk. Animals fed

> identical diets differing only in the type of starch (high or low

> glycemic index) gain body fat faster on the high glycemic index

diet

> [52••]. Even when fed to similar body weight, the high glycemic

index-

> fed rats had more body fat (+71%), less lean body mass and higher

> plasma triglyceride concentrations. In addition, high glycemic

index

> feeding was associated with significant disruption of [beta]-cell

> architecture after only 18 weeks.

>

> Mechanisms of hyperglycemia-induced endothelial damage

> Several molecular mechanisms have been implicated in glucose-

> mediated vascular damage. All appear to reflect a single

> hyperglycemia-induced process of overproduction of superoxide by

the

> mitochondrial electron-transport chain. The vascular endothelium is

a

> prime target because endothelial cells, unlike many other cells in

> the body, are unable to regulate glucose transport across the cell

> membrane [53]. Normal levels of glycemia encountered during an oral

> glucose tolerance test or standard meal have been shown to acutely

> decrease plasma antioxidant capacity, reflecting a significant

level

> of oxidative stress [54•]. Damage to the endothelium caused by high

> blood glucose levels may play an important role in the development

of

> atherosclerosis. Upregulation of inflammatory transcription factors

> such as nuclear factor-[kappa]B is an early marker of endothelial

> dysfunction [55,56•]. Moderately elevated CRP, a sensitive

surrogate

> marker for low-level inflammation, has been linked to insulin

> resistance, obesity and hyperglycemia [57•], and more recently to

the

> glycemic index and glycemic load of the diet. In 244 healthy,

middle-

> aged women, a high dietary glycemic load independently predicted

> elevated plasma concentrations of CRP with a two-fold increase

> comparing the lowest and the highest quintiles [30]. In lean young

> volunteer studies, we found the strongest independent predictor of

> fasting CRP concentration was the 120 min blood glucose levels

> following a carbohydrate challenge (S. Dickinson, J. Brand-,

> unpublished data).

>

> Conclusion

> Taken together, observational, interventional and experimental

> studies suggest that nondiabetic levels of postprandial glycemia

may

> play a greater role in CVD than is generally acknowledged. Rapidly

> absorbed carbohydrates and diets with a high glycemic load lead to

> the highest levels of postprandial blood glucose. Recommendations

to

> reduce saturated fat and increase carbohydrate intake have

> inadvertently encouraged greater consumption of high glycemic index

> foods and thereby increased day-long glycemia. The evidence that

this

> may be harmful is stronger in individuals with higher BMI, insulin

> resistance or impaired glucose tolerance. However, even so-called

> normal levels of post-meal glycemia may not be as benign as we take

> for granted.

> It may therefore be timely to give greater consideration to the

> glycemic potential (glycemic index) of dietary carbohydrate in

> dietary recommendations. Current emphasis on increasing wholegrains

> and restriction of sugar, although helpful from a micronutrient

point

> of view, is unlikely to improve glycemia. Furthermore, it may

> alienate and discourage some consumers from adopting more effective

> dietary strategies to reduce the risk of chronic disease.

Encouraging

> greater consumption of low glycemic index foods, however, will

> require local and brand-specific knowledge of the glycemic index of

> breads, breakfast cereals, rices and other cereal products.

>

> References and recommended reading

> Papers of particular interest, published within the annual

period

> of review, have been highlighted as:

> • of special interest

> •• of outstanding interest

>

> 1• Gross L, Li L, Ford E, Liu S. Increased consumption of refined

> carbohydrates and the epidemic of type 2 diabetes in the United

> States: an ecologic assessment. Am J Clin Nutr 2004; 79:774–779.

This

> ecological correlation study confirms that the American diet has

> increased dramatically in refined carbohydrate. The analysis

revealed

> a positive significant association between refined carbohydrate and

> prevalence of type 2 diabetes. [Context Link]

> 2• Schulze M, Liu S, Rimm E, et al. Glycemic index, glycemic load,

> and dietary fiber intake and incidence of type 2 diabetes in

younger

> and middle-aged women. Am J Clin Nutr 2004; 80:348–356. This follow-

> up study examined a cohort from the Nurses' Health Study II and

found

> that after adjusting for common confounders, glycemic index was

> significantly associated with increasing risk for diabetes while

> cereal fiber was associated with a decrease risk. [Context Link]

> 3 Liu S, Willett W, Stampfer M, et al. A prospective study of

dietary

> glycemic load, carbohydrate intake, and risk of coronary heart

> disease in US women. Am J Clin Nutr 2000; 71:1455–1461.

Bibliographic

> Links [Context Link]

> 4 - K, Holt SH, Brand- JC. International table of

> glycemic index and glycemic load values. Am J Clin Nutr 2002; 76:5–

> 56. Bibliographic Links [Context Link]

> 5 Augustin L, Franceschi S, D, et al. Glycemic index in

> chronic disease: a review. Eur J Clin Nutr 2002; 56:1049–1071.

> Bibliographic Links [Context Link]

> 6•• Sheard N, N, Brand- J, et al. Dietary Carbohydrate

> (amount and type) in the Prevention and Management of Diabetes: A

> statement by the American Diabetes Association. Diabetes Care 2004;

> 27:2266–2271. This important statement by the American Diabetes

> Association acknowledges the use of the glycemic index as a means

to

> help regulate blood glucose levels, offering additional benefits

over

> simply considering total dietary carbohydrate alone. [Context Link]

> 7 D, Zimmet P, Welborn T, et al. The rising prevalence of

> diabetes and impaired glucose tolerance: the Australian Diabetes,

> Obesity and Lifestyle Study. Diabetes Care 2002; 25:829–834.

> Bibliographic Links [Context Link]

> 8• Wild S, Roglic G, Green A, et al. Global prevalence of diabetes:

> estimates for the year 2000 and projections for 2030. Diabetes Care

> 2004; 27:1047–1053. This study reports on the current global

epidemic

> of diabetes. New data and methods are used to estimate age-specific

> prevalence across 191 World Health Organization member states for

the

> year 2000 and 2030. [Context Link]

> 9 Treuth M, Sunehag A, Trautwein L, et al. Metabolic adaptation to

> high-fat and high-carbohydrate diets in children and adolescents.

Am

> J Clin Nutr 2003; 77:479–489. Bibliographic Links [Context Link]

> 10• Atkinson F, McMillan-Price J, Petocz P, Brand- J.

> Physiological validation of the concept of glycemic load in mixed

> meals over 10 hours in overweight females. Proc Nutr Soc Aust 2004;

> 13:S42. This intervention, crossover study examined day-long

glucose

> and insulin responses from four isoenergetic reduced fat diets. The

> glycemic load of the mixed meals produced predictable orders of

> response. [Context Link]

> 11•• Brynes A, Mark EC, Ghatei M, et al. A randomised four-

> intervention crossover study investigating the effect of

> carbohydrates on daytime profiles of insulin, glucose, non-

esterified

> fatty acids and triacylglycerols in middle-aged men. Br J Nutr

2003;

> 89:207–218. Buy Now Bibliographic Links This intervention crossover

> study of four different diets provides strong evidence that CVD

risk

> factors can be reduced through dietary manipulation. Significant

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> 15 The DECODE Study Group. Glucose tolerance and mortality:

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> 18 Temelkova-Kurktschiev T, Koehler C, Henkel E, et al.

Postchallenge

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> 19 Hanefeld M, Koehler C, Schaper F, et al. Postprandial plasma

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> 20•• nsen L, Jenssen T, Joakimsen O, et al. Glycated

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> Circulation 2004; 110:466–470. This study is the first to report on

> the relationship between glycated hemoglobin and carotid intima-

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> cholesterol concentration among US adults. Arch Intern Med 2001;

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> high glycemic load and plasma concentrations of high-sensitivity C-

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> 498. Bibliographic Links [Context Link]

> 31• Harbis A, Perdreau S, -Baudry S, et al. Glycemic and

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rich

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> Framingham Offspring Cohort. Diabetes Care 2004; 27:538–546.

> Bibliographic Links An excellent study showing that dietary

glycemic

> index and glycemic load are associated with lower insulin

resistance

> (HOMA-IR). The association between glycemic index, glycemic load

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> insulin resistance remained after adjusting for cereal fiber and

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> dietary glycemic load and overall glycemic index in a population of

> young children. While no significant associations between glycemic

> index, glycemic load and BMI were noted the overall glycemic index

> was positively associated with serum insulin concentrations.

[Context

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> 1987; 46:66–71. Bibliographic Links [Context Link]

> 35 Frost G, Leeds A, Trew G, et al. Insulin sensitivity in women at

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diet.

> Metabolism 1998; 47:1245–1251. Bibliographic Links [Context Link]

> 36• Patel V, Aldridge R, Leeds A, et al. Retrospective analysis of

> the impact of a low glycaemic index diet on hospital stay following

> coronary artery bypass grafting: a hypothesis. J Hum Nutr Diet

2004;

> 17:241–247. This retrospective study found that hospital patients

> consuming a low glycemic index diet prior to surgery were more

> insulin sensitive and had improved postprandial glycemia. Length of

> hospital stay was significantly reduced in this group. [Context

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> 37•• Sloth B, Krog-Mikkelsen I, Flint A, et al. No difference in

body

> weight decrease between a low-glycemic-index and a high-glycemic-

> index diet but reduced LDL cholesterol after 10-wk ad libitum

intake

> of the low-glycemic-index diet. Am J Clin Nutr 2004; 80:337–347. An

> excellent study that investigated the long-term effects of a low-

fat,

> high-carbohydrate diet with either low or high glycemic index

> carbohydrate treatments. Interestingly, while there was no

difference

> in weight loss between the groups, LDL cholesterol was reduced on

the

> low glycemic index diet. [Context Link]

> 38•• Opperman A, Venter C, Oosthuizen W, et al. Meta-analysis of

the

> health effects of using the glycaemic index in meal-planning. Br J

> Nutr 2004; 92:367–381. A meta-analysis of 16 research papers

> supporting the use of glycemic index for total cholesterol

reduction

> and the improvement of metabolic control for people with diabetes.

> [Context Link]

> 39•• Chiasson J, Josse R, Gomis R, et al. Acarbose treatment and

the

> risk of cardiovascular disease and hypertension in patients with

> impaired glucose tolerance: the STOP-NIDDM trial. JAMA 2003;

290:486–

> 494. An important intervention study producing direct evidence for

> the first time that reducing postprandial hyperglycemia, by slowing

> carbohydrate absorption in the gut (and thus mimicking the effect

of

> low glycemic index carbohydrate), substantially reduces the risk

for

> cardiovascular events among patients with IGT even after adjusting

> for conventional risk factors. [Context Link]

> 40• Hanefeld M, Chiasson J, Koehler C, et al. Acarbose slows

> progression of intima-media thickness of the carotid arteries in

> subjects with impaired glucose tolerance. Stroke 2004; 35:1073–

1078.

> This study also involved participants from the STOP-NIDDM trial.

The

> authors went a step further from the above work and found that

> acarbose treatment was associated with a 50% annual reduction in

the

> progression of intima-media thickening, a surrogate marker for

> atherosclerosis. [Context Link]

> 41 Campfield L, F. Blood glucose dynamics and control of meal

> initiation: a pattern detection and recognition theory. Physiol Rev

> 2003; 83:25–58. Bibliographic Links [Context Link]

> 42 Ludwig D. Dietary glycemic index and obesity. J Nutr 2000;

> 130:280S–283S. Bibliographic Links [Context Link]

> 43 Warren J, Henry C, Simonite V. Low glycemic index breakfasts and

> reduced food intake in preadolescent children. Pediatrics 2003;

> 112:e414. [Context Link]

> 44 Febbraio M, Keenan J, Angus D, et al. Preexercise carbohydrate

> ingestion, glucose kinetics, and muscle glycogen use: effect of the

> glycemic index. J Appl Physiol 2000; 89:1845–1851. Bibliographic

> Links [Context Link]

> 45 Kirwan J, Cyr- D, W, et al. Effects of moderate

> and high glycemic index meals on metabolism and exercise

performance.

> Metabolism 2001; 50:849–855. Bibliographic Links [Context Link]

> 46 Agus M, Swain J, Larson C, et al. Dietary composition and

> physiologic adaptations to energy restriction. Am J Clin Nutr 2000;

> 71:901–907. Bibliographic Links [Context Link]

> 47 Bouche C, Rizkalla S, Luo J, et al. Five-week, low-glycemic

index

> diet decreases total fat mass and improves plasma lipid profile in

> moderately overweight nondiabetic men. Diabetes Care 2002; 25:822–

> 828. Bibliographic Links [Context Link]

> 48 Ebbeling C, Leidig M, Sinclair K, et al. A reduced-glycemic load

> diet in the treatment of adolescent obesity. Arch Pediatr Adolesc

Med

> 2003; 157:773–779. Bibliographic Links [Context Link]

> 49 Spieth L, Harnish J, Lenders C, et al. A low-glycemic index diet

> in the treatment of pediatric obesity. Arch Pediatr Adolesc Med

2000;

> 154:947–951. Bibliographic Links [Context Link]

> 50• Stern L, Iqbal N, Seshadri P, et al. The effects of low-

> carbohydrate versus conventional weight loss diets in severely

obese

> adults: one-year follow-up of a randomized trial. Ann Intern Med

> 2004; 140:778–785. Bibliographic Links This randomized trial

compared

> weight loss in severely obese patients consuming a conventional

> weight loss diet versus a low-carbohydrate diet over a 1-year

period.

> Although drop out rates were high and the results may not be

> applicable to moderately overweight individuals, the low-

carbohydrate

> diet produced greater weight loss and a more favorable blood lipid

> profile. [Context Link]

> 51•• Yancy W, Olsen M, Guyton J, et al. A low-carbohydrate,

ketogenic

> diet versus a low-fat diet to treat obesity and hyperlipidemia: a

> randomized, controlled trial. Ann Intern Med 2004; 140:769–777.

This

> well controlled intervention study shows that a low-carbohydrate

diet

> seems to be more effective for treating obesity and hyperlipidemia

> compared with a conventional low-fat approach over a 24-week

period.

> LDL cholesterol, however, was slightly higher on the low-

carbohydrate

> diet. = http://tinyurl.com/4fxzj

> 52•• Pawlak DB, Kushner JA, Ludwig DS. Effects of dietary glycaemic

> index on adiposity, glucose homoeostasis, and plasma lipids in

> animals. The Lancet 2004; 364:778–785. A very well designed and

> controlled animal study demonstrating the beneficial effects of a

low

> versus high glycemic index diet on body composition and risk

factors

> for diabetes and cardiovascular disease. The strengths lie in their

> controlling of potential confounding factors that arise through

> manipulation of dietary glycemic index. Macronutrient,

micronutrient

> and fiber content were identical in the two diets while food

amounts

> were adjusted to maintain the same mean body weight in the groups.

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> 53 Brownlee M. Biochemistry and molecular cell biology of diabetic

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> 2095. An excellent review which argues that total glycemic exposure

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> CRP produced proatherogenic effects which were significantly

> amplified under hyperglycemic conditions.

[Guest guest]

Hi Rodney, did somebody mention starch? Very interesting paper

posted by Alan, I think it is the shape of things to come. Well, I

have now cut out all starch and my allergy has gone. But I have

noticed a few others things along the way, one, not connected as

such is that the removal of all the salt from the bread has lowered

my blood pressure significantly from 122/76 at its most saltiest to

105/59 at its least saltiest.

Anyway, first I use to eat oats or bread with every meal and after

the meal (about an hour and half later) I would get really sleepy,

just like a wave of tiredness washed over me, then another hour and

it would pass (I get this feeling with wine, but quicker and its

probably because I am not use to alcohol).

Secondly I, at age 34, started getting slightly blurred vision if

reading text, got my eyes checked out and they said I could have

glasses for reading if I wished, but it was up to me. So I decided

not to bother for then and worked on reducing grains. Now the

problem has gone, no more blurred vision, again since the grains

went.

Thirdly I did test my blood glucose after meals when eating bread

and oats and it would often reach its maximum for me (5.9 in UK

figures, think that's about 110 in American figures). Now my mother

is also a bread-head like I was, 24 years older than me and she is

getting blood glucose readings between meals in the 7.0-8.0 (130-

150) range. And that I guess would be my future if I had not dumped

the starchy grains.

Fourthly, twice in the past 4 months my partner has had bad colds

and two stomach bugs, without fail I get them too and they are

always bad, I get wretched sore throats and fever and the whole

thing passes through me like a train (in and out in 72 hours).

Well, since I removed starch on both occasions of her colds I also

got a little dryness in my throat and this lasted about seven hours

and was gone. It actually happened today, and last night my partner

did not get a wink of sleep as her nose was streaming etc. So colds

and bugs are trying to get through my immune defences but just

failing (I do also get more natural vit C now, maybe 900mg a day

from fruit and veg compared with 350mg before).

Now I have calorie restricted for about 13 years (first with zero

attempt at the ON bit, then with CRAN then in last five years with

CRON, but I never really felt the benefits, still had allergy and on

average seven colds a year, 2-3 being really bad fevers. But now I

feel invincible, I really feel as if the calorie restriction with ON

was worth the effort, I've waited over ten years to actually feel

healthy, the colds, flu and stomach bugs going around have not

touched me even though I made no attempt to avoid contact with my

partner etc. I feel more alert, less sleepy. Now some of these

benefits are probably due to allergy removal, but others I am sure

are starch related in the sense that my blood sugars are on average

much lower as I don't spike very high at all now in my bread and

grainless world.

My only concern now is can you have too much fruit, anybody know any

studies saying fruit can mess with blood glucose levels in a

dangerous way ? as once the spring comes I could drop my fat to 25%

of calories with extra fruit availability, but all this talk of

blood glucose these days makes me wonder if fruit is truly benign.

richard .....

[Guest guest]

Hi :

My only half-educated suggestion is to eat the fruits for which there

is clear evidence of benefit. Most fruits contain a sizeable number

of calories (from sugar) with, apart from vitamin C, few

micronutrients.

Most beneficial ............. well make up your own list, but you

might want to use anti-oxidant capacity as one important criterion -

I believe you will find lists in the files here. My list includes

tomatoes, prunes, and berries of all kinds. But I can't resist

things like apricots and peaches in season.

Once years ago I did calculations of six key nutrients per 100

calories for a very wide range of foods. Apples, as an example,

largely because of the sugar content, came VERY low on the list. Not

joking, they came out below 'bacon double cheeseburger' and not far

above 'salt pork'. Perhaps that was because of the choice of six

nutrients (vitamins C and E and folic acid; and Ca, K and one other

element, I forget which). In any event I tend to not go hog-wild on

the sugary fruits.

Suggestions better informed than mine above (doubtless not difficult)

will be appreciated.

Rodney.

>

>

> Hi Rodney, did somebody mention starch? Very interesting paper

> posted by Alan, I think it is the shape of things to come. Well, I

> have now cut out all starch and my allergy has gone. But I have

> noticed a few others things along the way, one, not connected as

> such is that the removal of all the salt from the bread has lowered

> my blood pressure significantly from 122/76 at its most saltiest to

> 105/59 at its least saltiest.

>

> Anyway, first I use to eat oats or bread with every meal and after

> the meal (about an hour and half later) I would get really sleepy,

> just like a wave of tiredness washed over me, then another hour and

> it would pass (I get this feeling with wine, but quicker and its

> probably because I am not use to alcohol).

>

> Secondly I, at age 34, started getting slightly blurred vision if

> reading text, got my eyes checked out and they said I could have

> glasses for reading if I wished, but it was up to me. So I decided

> not to bother for then and worked on reducing grains. Now the

> problem has gone, no more blurred vision, again since the grains

> went.

>

> Thirdly I did test my blood glucose after meals when eating bread

> and oats and it would often reach its maximum for me (5.9 in UK

> figures, think that's about 110 in American figures). Now my mother

> is also a bread-head like I was, 24 years older than me and she is

> getting blood glucose readings between meals in the 7.0-8.0 (130-

> 150) range. And that I guess would be my future if I had not

dumped

> the starchy grains.

>

> Fourthly, twice in the past 4 months my partner has had bad colds

> and two stomach bugs, without fail I get them too and they are

> always bad, I get wretched sore throats and fever and the whole

> thing passes through me like a train (in and out in 72 hours).

> Well, since I removed starch on both occasions of her colds I also

> got a little dryness in my throat and this lasted about seven hours

> and was gone. It actually happened today, and last night my

partner

> did not get a wink of sleep as her nose was streaming etc. So

colds

> and bugs are trying to get through my immune defences but just

> failing (I do also get more natural vit C now, maybe 900mg a day

> from fruit and veg compared with 350mg before).

>

> Now I have calorie restricted for about 13 years (first with zero

> attempt at the ON bit, then with CRAN then in last five years with

> CRON, but I never really felt the benefits, still had allergy and

on

> average seven colds a year, 2-3 being really bad fevers. But now I

> feel invincible, I really feel as if the calorie restriction with

ON

> was worth the effort, I've waited over ten years to actually feel

> healthy, the colds, flu and stomach bugs going around have not

> touched me even though I made no attempt to avoid contact with my

> partner etc. I feel more alert, less sleepy. Now some of these

> benefits are probably due to allergy removal, but others I am sure

> are starch related in the sense that my blood sugars are on average

> much lower as I don't spike very high at all now in my bread and

> grainless world.

>

> My only concern now is can you have too much fruit, anybody know

any

> studies saying fruit can mess with blood glucose levels in a

> dangerous way ? as once the spring comes I could drop my fat to 25%

> of calories with extra fruit availability, but all this talk of

> blood glucose these days makes me wonder if fruit is truly benign.

>

> richard .....

[Guest guest]

PS:

I also go through a couple of lemons a week in tea.

Rodney.

> >

> >

> > Hi Rodney, did somebody mention starch? Very interesting paper

> > posted by Alan, I think it is the shape of things to come. Well,

I

> > have now cut out all starch and my allergy has gone. But I have

> > noticed a few others things along the way, one, not connected as

> > such is that the removal of all the salt from the bread has

lowered

> > my blood pressure significantly from 122/76 at its most saltiest

to

> > 105/59 at its least saltiest.

> >

> > Anyway, first I use to eat oats or bread with every meal and

after

> > the meal (about an hour and half later) I would get really

sleepy,

> > just like a wave of tiredness washed over me, then another hour

and

> > it would pass (I get this feeling with wine, but quicker and its

> > probably because I am not use to alcohol).

> >

> > Secondly I, at age 34, started getting slightly blurred vision if

> > reading text, got my eyes checked out and they said I could have

> > glasses for reading if I wished, but it was up to me. So I

decided

> > not to bother for then and worked on reducing grains. Now the

> > problem has gone, no more blurred vision, again since the grains

> > went.

> >

> > Thirdly I did test my blood glucose after meals when eating bread

> > and oats and it would often reach its maximum for me (5.9 in UK

> > figures, think that's about 110 in American figures). Now my

mother

> > is also a bread-head like I was, 24 years older than me and she

is

> > getting blood glucose readings between meals in the 7.0-8.0 (130-

> > 150) range. And that I guess would be my future if I had not

> dumped

> > the starchy grains.

> >

> > Fourthly, twice in the past 4 months my partner has had bad colds

> > and two stomach bugs, without fail I get them too and they are

> > always bad, I get wretched sore throats and fever and the whole

> > thing passes through me like a train (in and out in 72 hours).

> > Well, since I removed starch on both occasions of her colds I

also

> > got a little dryness in my throat and this lasted about seven

hours

> > and was gone. It actually happened today, and last night my

> partner

> > did not get a wink of sleep as her nose was streaming etc. So

> colds

> > and bugs are trying to get through my immune defences but just

> > failing (I do also get more natural vit C now, maybe 900mg a day

> > from fruit and veg compared with 350mg before).

> >

> > Now I have calorie restricted for about 13 years (first with zero

> > attempt at the ON bit, then with CRAN then in last five years

with

> > CRON, but I never really felt the benefits, still had allergy and

> on

> > average seven colds a year, 2-3 being really bad fevers. But now

I

> > feel invincible, I really feel as if the calorie restriction with

> ON

> > was worth the effort, I've waited over ten years to actually feel

> > healthy, the colds, flu and stomach bugs going around have not

> > touched me even though I made no attempt to avoid contact with my

> > partner etc. I feel more alert, less sleepy. Now some of these

> > benefits are probably due to allergy removal, but others I am

sure

> > are starch related in the sense that my blood sugars are on

average

> > much lower as I don't spike very high at all now in my bread and

> > grainless world.

> >

> > My only concern now is can you have too much fruit, anybody know

> any

> > studies saying fruit can mess with blood glucose levels in a

> > dangerous way ? as once the spring comes I could drop my fat to

25%

> > of calories with extra fruit availability, but all this talk of

> > blood glucose these days makes me wonder if fruit is truly benign.

> >

> > richard .....