Type
2 diabetes mellitus (T2DM) is a highly lifestyle-dependent metabolic disease. Its
global prevalence is predicted to reach 300 million by 2025, increasing
concomitant with obesity and the global adoption of a sedentary lifestyle. This
has worrying public health and economic implications (Hussain,
Claussen, Ramachandran, & Williams, 2007).
Atkins’
Nutritional Approach (ANA) is a low-carbohydrate ketogenic diet (LCKD) for
weight loss. Protein and fat make up most of the calories in ANA (Atkins,
2002) (see Appendix A).
This
report describes T2DM, its conventional treatment, and discusses treatment using
ANA. The author describes his experiences of ANA, and records progress statistics
(body mass index (BMI) and waist circumference; see supporting document). The
document concludes with statements of reflection on the diet and on the
author’s learning experience.
T2DM
is characterised by hyperglycaemia, as diagnosed by elevated fasting plasma
glucose (FPG) and oral glucose tolerance testing (OGTT). Glycosylated
haemoglobin (HbA1C) tests are also used (American
Diabetes Association, 2011).
Symptoms of hyperglycaemia include
polyuria, thirst, blurred vision, weight loss, dry skin and fatigue. If
untreated, symptoms include ketoacidosis, coma and death (World Health
Organisation, 1998).
T2DM
complications produce major signs and symptoms (Figure 1).
Hyperglycaemia
is associated with insulin resistance, where body tissues produce a
weaker-than-normal response to a given amount of insulin.
This is accelerated by increased adiposity, causing increased insulin secretion
from pancreatic beta cells, and poor glycaemic control. Long term, this can
cause beta cell exhaustion, and relative insulin deficiency compared to demand (Kumar,
Abbas, Fausto, & Aster, 2010).
A primary risk factor for T2DM is
obesity (BMI >30; vide supra). Genetic
factors and family history also contribute, but the current epidemic is mostly caused
by excessive energy intake versus expenditure (Sladek et al., 2007).
Other risk factors include age,
hypertension, low HDL and high triglyceride concentrations, and polycystic
ovarian syndrome or gestational diabetes (National Centre for Biotechnology
Information, 2011).
T2DM contributes up to 95% of all
diabetes mellitus (DM) cases. Between
2000 and 2010 the Australian DM prevalence increased 33% (1.0 to 1.3 million) (Zimmet,
Alberti, & Shaw, 2001).
Aboriginal and Torres Strait Islander,
Polynesian, Micronesian, Indian and Chinese are at increased risk. In developed
countries, T2DM is more common in lower socioeconomic groups. Education is
implicated in this discrepancy. The reverse is true for developing countries
(Shaw & Chisholm, 2003).
Hyperglycaemia
causes T2DM complications, including nephropathy/renal failure, neuropathy,
foot ulcers, neuropathic arthropathy, retinopathy, blindness and hypertension
(Figure 1) (National Centre for Biotechnology Information, 2011). Cardiovascular
disease (CVD) and stroke incidences are also increased (World Health Organisation,
1998).
Complications
are common in unmanaged diabetics. The mortality rate of DM patients is
three times that of other Australians, and
T2DM is a leading cause of death in Australia (Australian
Institute of Health and Welfare, 2009; Australian Bureau of Statistics, 2006). Diabetics
have poor quality of life (Figure 2).
Diet and exercise are important
T2DM treatments, reducing incidence, complications and mortality (Pate et al., 1995).
Pharmaceuticals
are available (e.g. metformin, ascarbose and exogenous insulin) and most effective
when combined with lifestyle changes (American Diabetes Association, 2010).
Care
also involves counselling and teaching the patient to monitor blood glucose,
administer insulin, and maintain healthy weight (Figure 3).
Figure 3: Management
of T2DM (Ripsin, Kang, & Urban, 2009)
The principle of ANA (see
Appendix A) is that limiting dietary carbohydrates induces ketosis, similar to
prolonged starvation (Figure 4).
Limited dietary carbohydrate
lowers blood glucose, stimulating glucagon and suppressing insulin secretion.
This activates glycogenolysis in liver and skeletal muscle, maintaining blood
glucose until glycogen stores deplete. Suppressed
insulin secretion inhibits triacylglycerol (fat) deposition and stimulates lipolysis. Since
animals cannot synthesise glucose from fatty acids, ketone bodies become the
primary blood “transport molecule” for acetyl groups from lipolysis. This state
is called ketosis.
Gluconeogenesis synthesises glucose from glycerol/lactate/amino acids in the
liver. This glucose complements ketones in fuelling tissues (e.g. brain) that
cannot oxidise fat, and maintains blood glucose upon glycogen depletion. Erythrocytes
depend completely upon glucose (Westman, Mavropoulos, Yancy, & Volek, 2003).
Insulin
and blood glucose “spikes” are associated with high-carbohydrate meals, not
high-fat/protein meals, so LCKDs may improve glycaemic control (Hall, 2011). In
hyperglycaemia, glucose reacts with endogenous proteins, impairing their
function. This glycosylation is implicated in the pathogenesis of T2DM
complications, and may be reduced by lowered blood glucose in LCKDs (Kumar et
al., 2010).
Ketosis
involves lipolysis for energy production, and gluconeogenesis, an inefficient endothermic
process, to maintain blood glucose (Hall, 2011). These processes accelerate
weight loss, important in T2DM treatment. The inefficiency of gluconeogenesis can
allow weight loss despite excess caloric intake. Patients don’t feel
“constantly hungry” since calories aren’t restricted. Unlike starvation, loss
of muscle tissue is avoided by dietary protein and fat intake. Ketones suppress
appetite, so ANA also improves satiety (Westman et al., 2003).
Weight loss improves the
prognoses of T2DM patients, mainly through reducing insulin resistance, but
which diet to recommend is controversial (Davis,
Forbes, & Wylie-Rosett, 2009).
Conventional low glycaemic
index dietary treatments for T2DM comprise whole grains, fruit and vegetables,
complemented with omega-3 fatty acids and unsaturated fats (Hu & Willett, 2002; Mann, 2002).
ANA involves unrestricted fat
and protein intake, and small amounts of vegetables, fruits and whole grains
once healthy weight is achieved (see Figures 4 & 5) (Atkins, 2002).
Figure 6:
A "food pyramid" summarising scientifically accepted nutritional
guidelines (Harvard University School of Public Health, 2011)
American Diabetes Association
(2007) does not recommend LCKDs in T2DM management. However, LCKDs are effective
in weight loss and glycaemic control, increasing insulin sensitivity and
improving lipid profiles (HDL/LDL ratios increased, decreased total cholesterol
and triglyceride) for up to two years (Shai
et al., 2008; A. J. Nordmann et al., 2006). Yancy, Foy, Chalecki, Vernon, & Westman (2005) showed
that a 16-week LCKD significantly decreased glycosylated haemoglobin and
fasting blood glucose in T2DM patients (Figures 6 & 7).
Limited studies exist on long-term
safety of ANA. Ketogenic diets used to treat epilepsy reveal increased kidney
disease rates (Kossoff
et al., 2002). Brenner,
Meyer, & Hostetter (1982) implicated increased protein intake in
nephropathy. However, ANA
may alleviate some nephropathy by treating T2DM.
High
fat and protein intake may cause CVD (particularly atherosclerosis) long-term (Kavey
et al., 2003). One systematic review of LCKDs revealed no increase in CVD risk
factors (HDL/LDL) over one year (Dena M. Bravata et al., 2003). Other studies
showed improvement (Shai et al., 2008; A. J. Nordmann et al., 2006). In
contrast, overweight/obesity and CVD risk correlate strongly (Figure 8). Longer-term
studies are required.
Figure 9:
Population attributable risk percentage effects for overweight and obesity on
CVD risk factors and events in Framingham men and women followed up for 44
years (Wilson, D’Agostino, Sullivan, Parise, & Kannel, 2002)
Despite
unknown harms, physicians and patients may try ANA because of rapid (and
motivating) weight loss with increased satiety and unrestricted caloric intake,
and optimistic short-term trials.
Caution
should be exercised. Previous diabetes treatments (e.g. Avandia) were
associated with increased risk of CVD events once on the market, although, like
ANA, short-term trials were optimistic (Wooltorton, 2002). LCKDs can lower
blood glucose, so patients require supervision to prevent hypoglycaemia (Westman,
et al., 2003).
ANA is a controversial dietary therapy that may be used to
effectively treat T2DM and its complications. However, its potential risks do
not warrant its use over current conservative therapies.
Lifestyle interventions for T2DM require ongoing care and
support. The dieting process is physically and emotionally draining, and
information/support services would likely improve patient outcomes.
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Below is a summary of the
phases of ANA, as described in Atkins
(2002). Note: 1) that the author’s diet was that described in “Phase 1”, since
this represents the beginning of the programme and 2) that Atkins (2002)
encourages regular exercise and vitamin/mineral supplements to complement the
ANA
Phase
1 (“Induction”; at least two weeks – length depends on personal
preference):
-
Less
than 20g of daily carbohydrate,
chosen from vegetables and green salad (e.g. lettuce, small amounts of
broccoli; Atkins (2002) provides a list of allowed vegetables).
-
Liberal
fat and protein intake (e.g. fish, red meat, chicken, eggs). Cheeses are also
allowed.
-
Recommended
drink is water. Caffeine should be avoided but is allowed.
-
Alcoholic
beverages are prohibited.
-
Some
artificial sweeteners are allowed: sucralose is preferred.
-
Avocadoes,
olives, sour cream and full cream (unsweetened) are allowed in moderation,
though may curtail weight loss
Phase
2 (“Ongoing Weight Loss”; begins once approaching a comfortable
weight – designed to slow weight loss to allow more food options):
-
Add
5g of daily carbohydrate per week until no longer losing weight. The daily carbohydrate intake at this
point is the “Critical Carbohydrate Level for Losing” (CCLL)
-
A
list (“The Carbohydrate Ladder”) of carbohydrate-containing foods in the order
in which Dr Atkins advises they be introduced into the diet is provided in
Atkins (2002). The list is in order of increasing carbohydrate content
-
Phase
3 (“Pre-Maintenance”; begins once within 5-10 pounds (~0.5-1.0 kg) of
desired weight):
-
Add
10g of daily carbohydrate per week until weight gain begins, then cut back 10g. This is the “Critical Carbohydrate Level
for Maintenance” (CCLM)
-
Any
added food that promotes weight gain/cravings should be avoided
Phase
4 (“Life Maintenance”; begins once desired weight is reached and
CCLM is achieved):
-
Continue
eating at the CCLM, but try a variety of foods (in moderation) from the allowed
list in Atkins (2002). (Sugar is never allowed).
-
If
weekly weigh-ins reveal that weight is more than 5 pounds (~0.5 kg) above the
desired weight, Phase 1 is re-entered, followed by return to Phase 4 once
desired weight is returned.