Content uploaded by Folorunso Olabiyi
Author content
All content in this area was uploaded by Folorunso Olabiyi on Oct 11, 2016
Content may be subject to copyright.
Chapter 5
© 2013 Folorunso and Oguntibeju, licensee InTech. This is an open access chapter distributed under the
terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which
permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.
The Role of Nutrition in the Management
of Diabetes Mellitus
Olabiyi Folorunso and Oluwafemi Oguntibeju
Additional information is available at the end of the chapter
http://dx.doi.org/10.5772/48782
1. Introduction
Scientific evidence abound to show that the prevalence of diabetes mellitus(DM) is
increasing around the world at a rate that appears dramatic as to have been characterized as
an epidemic[1]. Among several factors that have been postulated to contribute to DM
epidemic, environmental factors have drawn particular attention because of the rapidity of
the increase in type 2 or the so called ‘maturity on- set’ diabetes mellitus. Nobuko Seike,
Mitsuhiko Noda and Takashi Kadowaki [2] evaluated the association between alcohol
consumption and the risk of type 2 DM, it was pointed out that type 2 diabetes mellitus is
closely related to life style factors including diet, physical activities, alcohol and smoking as
well as obesity and a family history of diabetes. According to the researchers, in Japan the
prevalence of diabetes mellitus both for men over age 50 and women over 60 well exceeds
10% and most have type 2 DM which is associated with excessive energy intake, lack of
physical exercise and obesity. In addition, Mayes and Botham[3] revealed that obesity –
particularly, abdominal obesity(a diet related disorder) is a risk factor for increased
mortality, hypertension, type 2 DM, hyperlipidaemia and various endocrine dysfunctions.
On the other hand, type 1 DM, or ’Juvenile DM’ or ‘insulin-dependent’ diabetes is less
common than type 2. Only 10% of all diabetics have type 1.
Type 1 diabetes occurs when the pancreas produces no insulin at all. It tends to emerge in
childhood or early adulthood (before the age of 40) and must be regulated by regularly
injecting insulin. Although the exact cause of type 1 diabetes is currently unknown, it is
widely believed that majority of type 1 diabetes is of the immune-mediated nature, where
beta cell loss is a T-cell mediated autoimmune attack [4].
With type 1 diabetes, the immune system attacks cells in the pancreas. This destroys or
damages them enough to stop the production of insulin. A number of experts attribute this
occurrence to a viral infection.
Diabetes Mellitus – Insights and Perspectives
84
Genetics are also thought to play a part in the cause of type 1 diabetes; it has often been seen
to run in families.
People who have a close relative (parent or sibling) with type 1 diabetes have a 6% chance of
developing type 1 diabetes too.
In some instances, type 1 diabetes can be caused by a condition of the pancreas known as
‘chronic pancreatitis’. Chronis pancreatitis causes an inflammation of the pancreas and can
cause serious damage to the cells that produce insulin [5].
It is a well known fact that DM being a metabolic, endocrine disorder is directly connected to
carbohydrate, lipid and protein metabolism. As a result, nutrition therapy forms an integral
part of diabetes management and diabetes self - management education. It is also well
established that diabetes is caused by either a lack of Insulin secretion or by insulin resistance.
The resultant disease or metabolic disturbance leads to hyperglycaemia and dyslipidemia in
the short term, as well as long term complications such as retinopathy, neuropathy and
nephropathy. Besides, persons with diabetes are 2 to 4 times more likely to develop coronary
artery disease or to suffer a stroke. Findings from the diabetic control and complication trials
(DCCT) and the United Kingdom prospective Diabetes study(UKPDS) clearly indicate that the
maintenance of near normal blood glucose level dramatically reduces the chronic
complications associated with this disorder. In addition, reducing elevated blood lipids levels
has been shown to lower the incidence of acute coronary events in other at-risk populations.
Research have shown that before the advent of insulin therapy in the early 20th century,
medical nutrition therapy (MNT) was the only form of therapy for DM[6].
However, there are many misconceptions concerning nutrition and diabetes [7]. Moreso,
most diabetics are confused with conflicting nutrition advice and opinions. And it is
commonly believed that diabetes cannot be completely cured , but it may be more easily
regulated and controlled with the right diet . With strict adherence to nutritionist’s advice,
diabetic patients may be able to significantly improve their quality of life. There is little data
on the role nutrition played in diabetes management in our environment, hence, the need
for a review like this.
2. Diabetes mellitus and nutrition
A number of nutritional factors have been found to influence the development of type 1
diabetes or type 1-related autoimmunity. One study has found, for example, that eating
vegetables daily during pregnancy reduced the risk of a child's developing type 1-associated
autoimmunity [8]. Another found that higher iron intake (via infant formula or
supplements) in the first four months of life was associated with a higher risk of developing
type 1 diabetes[9]. However, other studies have not found associations between diet and
type 1 diabetes development. For example, Virtanen et al.[10] found only a weak protective
effect of a few foods eaten during pregnancy and the development of type 1 related
autoimmunity in the offspring (those foods were butter, low-fat margarine, berries, and
coffee; most foods showed no association).
The Role of Nutrition in the Management of Diabetes Mellitus 85
2.1. Omega-3 fatty acids
Norris et al.[11] found that dietary intake of omega-3 fatty acids, found in fish, flax seeds,
walnuts, soy, canola, and greens, is protective against the development of type 1 diabetes-
related autoantibodies in children at genetic risk of type 1 diabetes. Omega-3s can reduce
inflammation, and the lack of omega-3s in Western diets may predispose people to
inflammation. Yet the same authors later found that omega-3 levels were not associated
with later development of type 1 in these children [12]. So, it is possible that omega-3s may
be protective against type 1 autoantibody development, but be less significant later in the
disease process.
An earlier study of the same children found that the mother's dietary intake of omega-3 fatty
acids during pregnancy did not affect the risk of autoimmunity in children [13]. Cod liver
oil, however, taken during pregnancy, has been associated with a reduced risk of type 1
diabetes in offspring. Both omega-3 fatty acids and vitamin D are present in this oil, and
either or both may play a role [14].
Virtanen et al.[15] found that the fatty acids associated with milk and ruminant meat fat
consumption were associated with an increased risk of type 1 related autoimmunity.
Linoleic acid, however, was associated with lower levels of autoimmunity, in children
genetically at risk of type 1 diabetes.
A group of people with metabolic syndrome (a group of conditions common in people with
type 1 or 2 diabetes) were given omega-3 fatty acid supplements or a placebo for six months.
Those taking the supplements were found to have lower markers of autoimmunity and
inflammation, as well as more weight loss, compared to people who did not take the
supplements [16].
Adequate intake of omega-3s during pregnancy may also decrease the risk of obesity in the
offspring. Higher levels of omega-6 fatty acids in relation to omega-3s in umbilical cord
blood has been associated with higher obesity in children at age 3 [17].
2.2. Chemicals and omega-3s
The presence of environmental contaminants in food may also play a role in the effects of
nutritional factors. Some contaminants may interfere with the beneficial effects of foods. For
example, in a study linking insulin resistance to persistent organic pollutants, the
researchers concluded that beneficial aspects of omega-3 fatty acids in salmon oil could not
counteract the harmful effects caused by the persistent organic pollutants in that oil [18].
Fish is one source of omega-3 fatty acids, but according to an editorial in the American Journal of
Clinical Nutrition (AJCN), it may be better to rely on plant-based sources instead [19]. Studies
on fish consumption and type 2 diabetes are inconsistent: some show that higher dietary
intake of omega 3s decreases the risk of type 2, some show no connection, and some even
show that higher fish consumption increases the risk of type 2 diabetes [20,21]. It may be that
the chemicals in fish can explain these inconsistencies. A study shows that plant-based omega
3s have different effects than marine-based omega 3s in relation to type 2 diabetes [22], it was
opined that this may be possibly due to the contaminants present in fish.
Diabetes Mellitus – Insights and Perspectives
86
A high fat diet, especially one high in saturated fats, has been linked to type 2 diabetes and
insulin resistance. It appears that saturated fatty acids (but not unsaturated fats) activate
immune cells, which produce an inflammatory protein, which in turn then makes cells more
insulin resistant [23].Mothers who consumed higher levels of trans fats had an increased
risk of excess body fat, and so did their breastfed infants [24].
Can the effects of a high fat diet be passed down to subsequent generations? In animal studies,
a high-fat diet that causes obesity in mothers can affect the metabolism and weight of her
offspring. But what about a high fat diet in fathers? In one study, the female offspring of
heavier father rats (fed a high-fat diet) had defects in their insulin and glucose levels, like their
fathers. Unlike their fathers, they were not heavier than the controls [25]. Other researchers fed
mice a high fat diet with fat composition similar to a standard Western diet, and then bred
them and fed them the same diet for multiple generations. Over four generations, the offspring
became gradually heavier, and developed higher insulin levels, despite not eating more
calories. The diet was associated with changes in gene expression [26].
2.3. Glycemic index and sweeteners
The glycemic index(GI) is a measurement of how high a certain food raises blood glucose
levels after it is eaten. Foods that have a high glycemic index will cause blood glucose to rise
more, triggering insulin production (in people who still produce insulin), then leading to
falling blood glucose levels. One prospective study has found that a higher glycemic index
diet leads to a faster progression to type 1 diabetes. The group of people on this diet,
however, did not have higher levels of autoantibodies, showing that the diet may affect
disease progression but not disease initiation. The mechanisms involved may include
oxidative stress, caused by high blood glucose levels after meals, or perhaps insulin
resistance. Whatever the mechanism, a high glycemic index diet may place additional stress
on beta cells that are already under an autoimmune attack [27].
Evidence favouring the active reduction of blood lipids continues to accumulate and several
major diabetes associations now recommend that diabetic patients should reduce fat intake
and increase carbohydrate intake to approximately 50% of total calories[1]. High fibre foods
has been advocated [28]. It was highlighted that, although before detailed advice can be
given, comparative data on the physiological effects of carbohydrate foods may be required.
The consumption of sugar-sweetened beverages has been associated with type 2 diabetes,
obesity, and metabolic syndrome. A meta-analysis of a 11 prospective studies (of over 300,000
people) found that those who consumed 1-2 sweetened beverages per day had a 26% greater
risk of developing type 2 diabetes than those who consumed fewer than one serving per
month. The risk was 20% higher for developing metabolic syndrome. Sugar-sweetened
beverages include soft drinks, fruit drinks, iced tea, and energy/vitamin water drinks [29].
High-fructose corn syrup is another sweetener linked to obesity. Rats given access to high-
fructose corn syrup gained more weight than those given access to sucrose, despite eating
the same number of calories [30].
The Role of Nutrition in the Management of Diabetes Mellitus 87
2.4. Zinc
A few studies have found that higher zinc levels in drinking water may be protective against
type 1 diabetes. For example, Zhao et al. [31], found that higher levels of zinc and magnesium
were associated with lower rates of type 1 diabetes in southwest England. In Norway, a study
found that higher zinc levels in water was associated with a lower risk of type 1 diabetes, but
the association was not statistically significant [32]. In Finland, a study found that low zinc
levels in drinking water was associated with a higher incidence of type 1 diabetes [33].
2.5. Nicotinamide and other antioxidants
Nicotinamide, is a component of vitamin B3 that has been shown to protect against diabetes
in animals, and prevent beta cell damage [34]. Even better, one study found that it
prevented the development of type 1 diabetes in children with type 1-associated
autoantibodies [35].
On the basis of these and other studies, a large, double-blind, placebo-controlled trial was
conducted in Europe, the U.S. and Canada, called the European Nicotinamide Diabetes
Intervention Trial (ENDIT). This trial gave nicotinamide to first degree relatives of people
with type 1 diabetes who already had developed type 1-associated autoantibodies.
Unfortunately, it found no difference in the development of diabetes between the two
groups during the 5 year follow-up period. The study gave high doses of the vitamin, up to
3 g/day (30-50 times higher than the RDA) [34].
Another double-blind, placebo controlled study in Sweden gave high doses of anti-oxidants
(including nicotinamide, vitamin C, vitamin E, Beta-carotene, and selenium) to people after
they were already diagnosed with type 1 diabetes and also found that they had no effect in
protecting the beta cells against the damage of free radicals [36]. There is no evidence
linking the anti-oxidants alpha- or beta-carotene levels and the development of type 1
related autoimmunity in another study as well [37].
Uusitalo et al. [38] also found that if pregnant women took anti-oxidants and trace minerals
(including retinol, beta-carotene, vitamin C, vitamin E, selenium, zinc, or manganese)
during pregnancy, there was no effect on the risk of the child's developing type 1-related
autoimmunity.
Czernichow et al.[39] found that anti-oxidant supplements were not protective against
metabolic syndrome, a group of conditions common in people with type 1 or 2 diabetes. Yet
they also found that the people who had the highest levels of some anti-oxidants (beta-
carotene, vitamin C, and vitamin E) in the beginning of the study, presumably due to a diet
rich in plant foods, did have a lower risk of developing metabolic syndrome.
While these studies did not find promising results concerning anti-oxidant supplements,
they also did not find that these supplements did any harm.
Free radicals may play a role in the inflammatory process that destroys the beta cells in type 1
diabetes [36]. Therefore, anti-oxidants have been thought to protect the body from oxidative
Diabetes Mellitus – Insights and Perspectives
88
stress due to the production of free radicals. But, there is some animal evidence that anti-
oxidant supplements may also increase insulin resistance, showing that the relationship may
not be so simple. When the researchers gave certain mice an anti-oxidant, they were more
likely to become insulin resistant [40]. Perhaps this finding could help explain why anti-
oxidant supplements have not been found to be protective against type 1 diabetes.
3. Food processing: AGEs
Advanced Glycation End products (AGEs)are found in heat processed foods and have been
linked to type 1 and type 2 diabetes in animal studies. They appear to predispose people to
oxidative stress and inflammation, and may affect the fetus if the mother consumes them
during pregnancy. A study has found that the level of AGEs that a mother eats are
correlated with insulin levels in the baby. It found that if mothers have high AGE levels, and
infant food is high in AGEs, it may raise the risk of diabetes in the offspring [41].
3.1. Protein
Researchers fed mother rats a diet that was deficient in protein, and found higher rates of
diabetes in the offspring. They also found that one of the offspring's genes was "silenced"-- a
gene associated with type 2 diabetes development. Nutrition, then, may have effects on gene
expression that are linked to type 2 diabetes development [42].
3.2. Nutritional management of DM
In contemporary time, Medical Nutrition Therapy (MNT) is used to describe dietary
prescriptions [43] .
MNT for diabetes aim to achieve the following objectives:
1. Achieve and maintain near normal blood glucose goals
2. Achieve and/ or maintain optimal blood lipid levels
3. Achieve and/ or maintain normal blood pressure
4. Prevent, delay or treat nutrition related complications
5. Provide adequate kcalories for achievement of reasonable body weight
6. Provide optimal nutrition for maximizing health and for growth, development,
pregnancy, and lactation
Body of knowledge shows that, with respect to carbohydrates, the key emphasis of MNT for
diabetes mellitus is on the total amount of carbohydrate in terms of energy intake [44].As far
as the type of carbohydrates to be ingested is concerned, the guidelines for MNT in DM
clearly stress the value of selecting vegetables, fruits and grains , so that the starches
consumed will include adequate amounts of both fibre and micronutrients[43].
Research findings shows specific interests in the role that dietary fiber may play in the
nutritional management of DM. Benefit of fiber were found with regard to glycaemic control,
HDL and LDL cholesterol and triacylglycerols [45]. However, a 3- month study by Jenkins et
The Role of Nutrition in the Management of Diabetes Mellitus 89
al.[46] did not find a metabolic advantage of high fiber over low fiber cereals. Also, a study
carried out by Erasmus et al. [47],showed that treatment with guar gum does not lower the
postprandial glucose level in both non- diabetic and diabetic Nigerian subjects.
3.3. Dietary principles for diabetes mellitus
The American Diabetes Association [7] gave the following guidelines:
3.3.1. Type 1 DM
Which can achieve much if the following dietary principles are observed ;
i. Integrate and syncronise with the time of action of insulin treatment – patient on insulin
therapy should eat at consistent time simultaneously with the time of action of insulin
preparation used. This will help to minimize the peak of blood glucose as well as
incidence of hypoglycaemia.
ii. Reduce saturated fat because diabetics are prone to having coronary heart disease and
dietary restriction may reduce the risk.
iii. Keep salt intake low: salt intake must be reduced by diabetics because it has high risk of
developing hypertension. However, intake of essential nutrients should be adequate
among growing patients.
iv. Exercise: For planned exercise, reduction in insulin dosage may be the preferred choice
to prevent hypoglycemia. Additional carbohydrate may be needed for unplanned
exercise. Moderate-intensity exercise increases glucose uptake by 2–3 mg · kg−1 · min−1
above usual requirements. Thus, a 70-kg person would need 8.4–12.6 g (10–15)
carbohydrate per hour of moderate physical activity. More carbohydrate would be
needed for intense activity.
v. Metabolic profile: Improved glycaemic control with insulin therapy is often associated
with increased body weight. Because of the potential for weight gain to adversely affect
glycaemia, lipids, blood pressure, and general health, prevention of weight gain is
desirable.
3.3.2. Type 2 DM
A change in dietary regimen has a greater potential to improve type 2 diabetes , therefore,
the following guidelines will serve a useful purpose.
Because many persons with type 2 diabetes are overweight and insulin resistant, medical
nutrition therapy should emphasize lifestyle changes that result in reduced energy intake
and increased energy expenditure through physical activity. Therefore, reducing body
weight by eating few calories and taking regular exercise. Also, increased physical activity
can lead to improved glycaemia, decreasing insulin resistance, and reduced cardiovascular
risk factors.
i. Reduce saturated fat and maintaining a reduced plasma low density lipoprotein
cholesterol levels.
Diabetes Mellitus – Insights and Perspectives
90
ii. Eating low glycaemic index foods such as soya beans, apple, grapefruits,
peas(groundnuts), increase intake of vegetables, fruits, legumes and whole grain cereal
that may mostly have low glycaemic indices.
iii. Keep salt intake low
iv. Fried food is not good for diabetes patients . Wheat bread, lean meat, game meat (bush
meat), green, leafy vegetables, garden egg, all these should be encouraged for DM
patients.
v. Physical activity: Increased physical activity can lead to improved glycaemia, decreased
insulin resistance, and reduced cardiovascular risk factors.
4. Epidemiological and laboratory studies
From the review by Kayode et al.(1), epidemiological studies (48) have reported that as
nations become more affluent, the nature of the people’s carbohydrate consumption changes
such that the ratio of complex (starches) to simple carbohydrates decreases. It has been
suggested that this change in dietary pattern is responsible for the occurrence of various
diseases, such as atherosclerosis, diabetes and hyperlipidaemia. One proposed physiological
basis underlying such suggestions is a traditionally held tenet that simple carbohydrates are
more readily available for immediate absorption by the gut than are more complex
carbohydrates and that they therefore produce a greater and faster rise in postprandial
plasma glucose and insulin responses than do the supposedly more gradually digested and
absorbed complex carbohydrate. Consequently, diets restricted in simple carbohydrates
have been recommended in disease states in which control of plasma glucose and/or insulin
is felt to be important. However, there is dearth of sufficient laboratory data to substantiate
the role nutrition plays in the management of diabetes mellitus.
4.1. Recommendations and further studies
To be able to effectively manage diabetes with the aid of dietary control, patient’s education,
understanding, and participation is vital since the complications of diabetes are far less
common and less severe in people who have well- managed blood glucose levels. Also,
there is reduction in expenses incurred due to this metabolic disorder which research shows
was a major drain on health and productivity – related resources of government and other
employers of labour.
Given the associated higher risks of cardiovascular disease, lifestyle modifications(which
includes smoking habits, sedentary life, lack of regular exercise etc,) are strongly
recommended. Besides, regular exercise, coupled with blood pressure , cholesterol levels,
body weight , HbA1C measurements is advocated among people with diabetes.
Omega-3 fatty acids may be protective against type 1 diabetes, but more studies would be
necessary to confirm this finding. Eating high glycemic-index foods may accelerate the
progression of type 1 diabetes, but this association should also be confirmed. Taking anti-
oxidant supplements does not appear to reduce the risk of type 1 diabetes, but it is possible
that a diet high in anti-oxidants may still be protective.
The Role of Nutrition in the Management of Diabetes Mellitus 91
More research is highly imperative on the epidemiological and laboratory aspects of the role
of nutrition in the management of diabetes mellitus.
Author details
Olabiyi Folorunso
Chemical Pathology Unit, Department of Medical Laboratory Science,
Achievers University, Owo, Nigeria
Oluwafemi Oguntibeju
Department of Biomedical Sciences, Faculty of Health & Wellness Sciences,
Cape Peninsula University of Technology, Bellville, South Africa
Acknowledgement
Our sincere appreciation goes to Professors S.A Shoyinka and J.I Anetor, for their invaluable
contributions.
5. References
[1] J. Kayode, A. Sola, A. Adelani, A. Adeyinka, O. Kolawole, O. Bashiru (2009): The role of
carbohydrate in diabetic nutrition: A review. The internet Journal of Laboratory
Medicine. Volume 3 Number 2.
[2] Nobuko Seike, Mitsuhiko Noda, Takashi Kadowaki (2009): Alcohol consumption and
the risk of type 2 diabetes mellitus in Japanese. A systematic review. Asia Pac J Clin
Nutr 17(4):545 – 551.
[3] Peter A. Mayes, Katleen M. Botham (2003): Lipid transport and storage . Harpers
illustrated Biochemistry. 26th Ed. Mc Graw Hill. 25: 205.
[4] Rother KI., (2007): ‘’Diabetes Treatment – bridging the divide ‘’. The New England
Journal of Medicine. 356(15):1499-501.
[5] Narendran P, Estella E, Fourlanos S, (2005): Immunology of type 1 diabetes.QJM. 547 -56.
[6] Blades M., Morgan J., Dickerson J., (1997) : Dietary advice in the management of
diabetes mellitus. history and current practice. J. R. Soc. Health 117: 143 – 150.
[7] American Diabetes Association (2004): Nutrition Principles and Recommendation in
Diabetes. Diabetic Care. Volume 27 no suppl 1536.
[8] Brekke HK., and Ludviqsson J., (2009) :Daily vegetable intake during pregnancy
negatively associated to islet autoimmunity in the offspring … the ABIS study. Pediatr
Diabetes. 4 : 244-50.
[9] Ashraf AP., Easson NB., Kabagambe EK., Haritha J., Meleth S., McCormic KL.,
(2010):Dietary iron intake in the first 4 months of infancy and the development of type 1
diabetes : a pilot study. Diabetol Metab Syndr 2:58.
[10] Virtanen SM., Uusitalo L., Kenwaed MG., Nevalainen J., Uusitalo U., Kronberg –Kippila
C., Ovaskainen ML., Arkkola T., Niinisto S., Hakulinen T., Ahonen S., Simeli O.,
Diabetes Mellitus – Insights and Perspectives
92
IlonenJ., Veijola R., Knip M., (2011) : maternal food consumption during pregnancy and
risk of advanced β-cell autoimmunityin the offspring. Pediatr Diabetes 12(2) : 95-9.
[11] Norris JM., Yin X., Lamb MM., Barriga K., Seifert J., Hoffman M., Orton HD., Baron AE.,
Clare-Salzler M., Chase HP., Szabo NJ., Erlich H., Eisenbarth GS., Rewers M., (2007):
Omega -3 polyunsaturated fatty acid intake and islet autoimmunity in children at
increased risk for type 1 diabetes. JAMA. 298(12):1420 -8.
[12] Miller MR., Yin X., Seifert J., Clare –Salzler M., Eisenbarth GS., Rewers M., Norris JM., (2011):
Erythrocyte membrane omega-3 fatty acid levels and omega -3 fatty acid intake are not
associated with conversion to type 1 diabetes in children with autoimmunity :the Diabetes
Autoimmunity Study in the young (DAISY). Pediatr Diabetes 12(8):669 -75.
[13] Fronczak CM., Baron AE., Chase HP., Ross C., Brady HL., Hoffman M., Eisenbarth GS.,
Rewers M., Norris JM., (2003) : In utero dietary exposures and risk of islet
autoimmunity in children. Diabetes Care. 26(12): 3237 - 42.
[14] Stene LC., Ulriksen J., Magnus P., Joner G., (2000) : Use of cod liver oil during
pregnancy associated with lower risk of type 1 diabetes in the offspring. Diabetologia.
43(9):1093 – 8.
[15] Virtanen SM., Niisisto S., Nevalainen J., Salminen I., Takkinen HM., Kaaria S., Uusitalo
L., Alfthan G., Kenward MG., Veijola R., Simeli O., Ilonen J., Knip M., (2010) : Serum
fatty acids and risk of advanced β-cell autoimmunity :a nested case – control study
among children with HLA – conferred susceptibility to type 1 diabetes. Eur J Clin Nutr
64(8) : 792 – 9.
[16] Ebrahimi M., Ghanyour –Mobarhan M., Rezaiean S., Hoseini M., Parizade SM.,
Farhoudi F., Hosseininezhad SJ., Tavallaaei S., Vejdani A., Azimi – Nezhad M., Shakeri
MT., Rad M., Mobara N., Kazemi – Bajestani SM., Ferns GA., (2009) : Omega – 3 fatty
acid supplements improve the cardiovascular risk profile of subjects with metabolic
syndrome including markers of inflammation and autoimmunity . Acta Cardiol
64(3) :321 -7.
[17] Donahue SM., Rifas – Shiman SL., Gold DR., Jouni ZE., Gillman MW., Oken E.,
(2011) :Prenatal fatty acid status and child adiposity at age 3y : results from a US
pregnancy cohort. Am J Clin Nutr 93(4):780 – 8.
[18] Ruzzin J., Petersen R., Mengnier E., Madsen L., Lock EJ., Lillefosse H., Ma T., Pesenti S.,
Soone SB., Marstrand TT., Malde MK., Du ZY., Chavey C., Fajas L., Lundebye AK.,
Brand CL., Vidal H., Kristiansen K., FrØyland L (2010) : Persistent organic pollutant
exposure leads to insulin resistance syndrome. Environ Health Perspect 18(4) : 465 -71.
[19] Feskens EJ., (2011):The prevention of type 2 diabetes. Should we recommend vegetable
oils instead of fatty fish? Am J Clin Nutr 94(2):369 -70.
[20] Djoussé L., Biggs ML., Lemaitre RN., Kings IB., Song X., Ix JH., Mukamal KJ., Siscovick
DS., Mozaffarian D.,(2011) :Plasma omega -3 faaty acids and incident diabetes in older
adults. Am J Clin Nutr 94(2) :527 – 33.
[21] Villegas R., Xiang YB., Elasy T., Li HL., Yang G., Cai H., Ye F., Gao YT., Shyr Y., Zheng
W., Shu XO., (2011) :Fish, shellfish, and long –chain n-3 fatty acid consumption and risk
of incident type 2 diabetes in middle –aged Chinese men and women. Am J Clin Nutr
94(2) :543- 51.
The Role of Nutrition in the Management of Diabetes Mellitus 93
[22] Brostow DP., Odegaard AO., Koh WP., Duval S., Gross MD., Yuan JM., Pereira MA.,
(2011): Omega – 3 fatty acids and incident type 2 diabetes : the Singapore Chinese
Health Study . Am J Clin Nutr 94(2): 520– 6.
[23] Wen H., Gris D., Lei Y., Jha S., Zhang L., Huang MT., Brickey WJ., Ting JP., (2011): Fatty
acid –induced NLRP3-ASC inflammation activation interferes with insulin signalling.
Nat Immunol 12(5):408 – 15.
[24] Anderson AK., McDougald DM., Steiner-Asiedu M., (2010) :Dietary trans fatty acid
intake and maternal and infant adiposity. Eur J Clin Nutr 64(11);1308 – 15.
[25] Ng SF., Lin RC., Laybutt DR., Barres R., Owens JA., Morris MJ., (2010): Chronic high –
fat diet in fathers programs β – cell dysfunction in female rat offspring. Nature. 21;
467(7318): 963 -6.
[26] Massiera F., Barbry P., Guesnet P., Joly A., Lugnet S., Moreilhon –Brest C., Mohsen –
Kanson T., Amri EZ., Ailhaud G.,(2010) : A Western – like fat diet is sufficient to induce
a gradual enhancement in fat mass over generations. J Lipid Res 51(8):2352-61.
[27] Lamb MM.,Yin X., Barriga K., Hoffman MR., Barón AE., Eisenbarth GS., Rewers M.,
Norris JM., (2008) : Dietary glycemic index , development of islet autoimmunity and
subsequent progression to type 1 diabetes in young children . J Clin Endocrinol metab
93(10):3936 -42.
[28] Jenkins DJA, Wolever TMS, Jenkins AL, Wong GS, Josse R. (1984): Glycaemic response
to carbohydrate foods. Lancet.388 -391.
[29] Malik VS.,Popkins BM., Bray GA., Pesprés JP., Willett WB., Hu FB., (2010):Sugar –
sweetened beverages and risk of metabolic syndrome and type 2 diabetes : a meta-
analysis. Diabetes Care. 33(11)2477 -83.
[30] Bocarsly ME., Powell ES., Avena NM., Hoebel BG., (2010): High fructose corn syrup
causes characteristic obesity in rats: increased body weight, body fat and triglyceride
levels. Pharmacol Biochem Behav 97(1):101 – 6.
[31] Zhao HX., Mold MD., Stenhouse EA., Bird SC., Wright DE., Demaine AG., Millward
BA., (2001): Drinking water composition and childhood – onset type 1 diabetes mellitus
in Devon and Cornwall England. Diabet Med 18(9): 709 - 17.
[32] Stene LC,Hongve D, Magnus P, RØnningen KS, Joner G (2002):Acidic drinking water
and risk of childhood –onset type 1 diabetes. Diabetes Care. 25(9) :1534 -8.
[33] Ulf S., Oikarinen S., Hyöty H., Ludvigsson J., (2011): Low Zinc in drinking water is
associated with the risk of type 1 diabetes in children. Pediatr Diabetes. 12(3 pt 1):156 – 64.
[34] Gale EA., Bingley PJ., Emmett CL., Collier T. (2004): European Nicotinamide Diabetes
Intervention Trial(ENDIT): a randomized controlled trial of intervention before the
onset of type 1 diabetes. Lancet. 363(9413):925 -31.
[35] Elliott RB., Pilcher CC., Fergusson DM., Stewart AW., (1996) :A population – based
strategy to prevent insulin –dependent diabetes using nicotinamide. J Pediatr
Endocrinol Metab 9(5): 501-9.
[36] Ludvigsson J., Samuelsson U., Johansson C., Sterhammar L., (2001) :Treatment with
antioxidant at onset of type 1 diabetes in children : a randomised double- blind placebo-
controlled study. Diabetes Metab Res Rev 17(2):131 -6.
Diabetes Mellitus – Insights and Perspectives
94
[37] Prassad M., Takkinen HM., Nevalainen J., Ovaskainen ML., Alfthan G., Uusitalo L.,
Kenward MG., Veijola R., Simell O., Ilonen J., Knip M., Virtanen SM., (2011): Are serum
α- anb β- carotene concentrations associated with the development of advanced β-cell
autoimmunity in children with increased genetic susceptibility to type 1 diabetes?
Diabetes Metab 37(2):162-7.
[38] Uusitalo L. Kenward MG. Virtanen SM., Uusitalo U., Nevalainen J., Niinistö S.,
Kronberg –Kippilä C., Ovaskainen ML., Marjamäki L., Simell O.,Ilonen J., Veijola R.,
Knip M.,(2008):Intake of antioxidant vitamins and trace elements during pregnancy and
risk of advanced beta cell autoimmunity in the child. Am J Clin Nutr 88(2):458-64.
[39] Czernichow S., Vergnaud AC., Galan P., Arnaud J., Favier A., Faure H., Huxley R.,
Hercberg S., Ahluwalia N., (2009): Effects of long term antioxidant supplementation
and association of serum antioxidant concentrations with risk of metabolic syndrome in
adults. Am J Clin Nutr 90(2):329 – 35.
[40] Loh K., Deng H., Fukushima A., Cai X., Boivin B., Galic S., Bruce C., Shields BJ., Skiba B.
Ooms LM., Stepto N., Wu B., Mitchell CA., Tonks NK., Watt MJ., Febbraio MA., Crack
PJ., Andrikopoulos S., Tiganis T., (2009) :Reactive oxygen species enhance insulin
sensitivity . Cell Memb 10(4) :260 -72.
[41] Mericq V., Piccardo C., Cai W., Chen X., Zhu L., Striker GE., Viassara H., Uribarri J.,
(2010): Maternally transmitted and food derived glycotoxins: a factor preconditioning
the young to diabetes? Diabetes Care. 33(10):2232-7.
[42] Sandovici I., Smith NH., Nitert MD., Ackers-Johnson M., Uribe-Lewis S., Ito Y., Jones
RH., Marguez VE., Cairns W., Tadayyon M., O’Neill Lp., Morrell A., Ling C.,
Constância M., Ozanne SE., (2011): Maternal diet and aging alter the epigenetic control
of a promoter enhancer interaction at the Hnf4a gene in rat pancreatic islet. Proc natl
Acad Sci 108(13):5449-54.
[43] American Diabetes Association (2002) :Evidence based Nutrition principles and
recommendations for the treatment and prevention of diabetes and related
complications. Diabetes Care. 25(suppl.): S50 -60.
[44] Kelly DE., (2003): Sugar and starch in the nutritional management of diabetes mellitus.
Am. J. Clin. Nutr. 78(suppl) :858S -864S.
[45] Chandalia M.,Garg A., Lutjohann D., Bergmann K., Grundy S., Brinkley L., (2000) :
Beneficial effects of high dietary fibre intake in patients with type 2 diabetes mellitus .
N.Eng. J. Med; 342: 1392 -1398.
[46] Jenkins D., Kendall C., Augustine L., Martini M., Axelsen M., Faulker D et al (2002):
Effect of wheat bran on glycaemic control and risk factors for cardiovascular disease in
type 2 diabetes .Diabetes Care;25:1522 – 1529.
[47] Erasmus RT., Adelowo D., Olukoga D., Okesina K., Medubi A., Adewoye H.,
(1988) :Effect of guar gum on glucose and lipid levels in healthy and non- insulin
dependent Nigerian diabetics. West Afr J Med; 7:45 -50.
[48] Crapo PA, Reaven G, Olefsky JM.( 1977): Postprandial glucose and insulin responses to
different complex carbohydrates. Diabetes; 26:1178-1183.
