The Facts
Diabetes Mellitus is an abnormal physiologic response to blood sugar and insulin. It is important to understand NORMAL physiology before we can understand how diabetes is abnormal.
Our blood sugar is controlled to a very narrow range. The normal range of blood glucose is 4.0-7.88mmol/L – these are important numbers to looks at. 
We start to have symptoms of true hypoglycemia. Hypoglycemia can be mild, moderate, or severe.

  • Mild Hypoglycemia: nausea, jittery/trembling, cold/clammy/wet skin, rapid heart beat (tachycardia)
  • Moderate Hypoglycemia: irritability/anxiety,
  • Severe Hypoglycemia.

Understanding Type I & Type II
We have a fairly good understanding of Diabetes these days. Every cell in your body needs sugar for energy, and sugar enters the cells through the action of insulin. When sugar can’t enter cells, it accumulates in the blood. 
There are three main lifestyle components to managing diabetes before turning to medication, and they are the cornerstones of treatment:

  • dietary changes
  • regular exercise
  • weight control

    **This information section is growing please check back.

Diabetes Mellitus – Type 1

Type 1 diabetes usually appears in childhood, and is caused by the body’s inability to produce insulin. Type 1 diabetes is the discovery (and production) of insulin transformed type 1 diabetes from a death sentence to a chronic illness. I’m also going to ignore the other forms of diabetes (e.g., gestational diabetes).
Type 1 Diabetes (T1D) mellitus is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin. Insulin, an anabolic hormone is produced by the beta cells of the islets of Langerhans located in the pancreas. The absence, destruction, or other loss of these cells results in type 1 or insulin-dependent diabetes mellitus (IDDM). Most children with diabetes have IDDM and a lifetime dependence on exogenous insulin.

T1D results from either the autoimmune destruction of the beta cells, possibly triggered by a viral infection (e.g., Coxsackie virus or other enteric virus) or by toxic exposure in a genetically susceptible individual. The progressive destruction takes place, in part, from T cell release of cytokines, which attack the beta cells. By the time a patient with T1D presents with symptoms, the pancreatic beta cells are 80% to 90% destroyed.

Normally insulin is essential to metabolise carbohydrates, fat, and protein. Insulin reduces blood glucose levels by allowing glucose to enter muscle cells and by stimulating the conversion of glucose to glycogen as a carbohydrate store (glycogenesis). Insulin also inhibits the release of stored glucose from liver glycogen (glycogenolysis) and slows the breakdown of fat to triglycerides, free fatty acids, and ketones.  It also stimulates fat storage. Additionally, insulin inhibits the breakdown of protein and fat for glucose production (gluconeogenesis) in both liver and kidneys. These metabolic balances are lost without insulin release in T1D.

Hyperglycaemia (i.e. random blood glucose concentration more than 11 mmol/L) result when insulin deficiency leads to uninhibited gluconeogenesis and prevents the use and storage of circulating glucose. The kidneys cannot reabsorb the excess glucose load, causing glycosuria, osmotic diuresis, thirst, and dehydration. Increased fat and protein breakdown leads to ketone production and weight loss. Without insulin, a child with IDDM wastes away and eventually dies from diabetic ketoacidosis (DKA).

Aetiology / Risk factors

  • Family history of type 1 diabetes
  • Mother who had preeclampsia during pregnancy
  • Family history of immune diseases including Hashimoto’s thyroiditis, Graves’ disease, myasthenia gravis, Addison’s disease, or pernicious anaemia
  • Illness during early infancy
  • Child of an older mother
  • Northern European or Mediterranean descent
  • Cow’s milk consumption in infancy (controversial): one study found that children exposed to cow’s milk during the first 8 days of life had two times the risk of developing type 1 diabetes compared to newborns receiving breast milk alone.

Signs and Symptoms
While destruction of beta cells occurs gradually, the following symptoms generally appear quite abruptly once 80% to 90% of the pancreatic beta cells are destroyed:

  • Polyuria, polydipsia, and/or polyphagia
  • Enuresis in children after they had already been adequately and appropriately trained
  • Unintended weight loss over several days; habitus is generally normal or wasted
  • Hyperglycaemia and glycosuria
  • Weakness and excessive fatigue
  • Increased susceptibility to infection, such as vaginitis and candida infections
  • Dehydration
  • Blurred vision
  • Irritability; restlessness; apathy
  • Nausea and vomiting
  • Ketoacidosis

Diet and Lifestyle

  • The diet should ideally be managed around regular blood sugar monitoring, and insulin intake. Following the principles of a balanced healthy regime to include at least 5 servings of vegetables, quality protein, reducing high glycaemic load foods, and to consume essential fatty acids (via nuts, seeds and fish) are all detailed in the Wellness and Healthy Ageing Program.
  • Smoking cessation is the highest priority in currently smoking patients.
  • Regular aerobic exercise (starting slowly and increasing as patient’s fitness improves) has been shown to stimulate non-insulin dependent glucose transport into cells.
  • Strategies to manage hypertension, lipids and obesity, as there is increased tendency to cardiovascular disease.
  • Patients with kidney damage should carefully monitor and in many cases moderate protein intake.

Diabetes Mellitus – Type 2

Type 2 diabetes is different. Either the cells are insensitive to insulin, or the body does not make enough to lower blood sugar – or it may be a combination of both effects. Type 2 diabetes is predominantly a disease of older adults. Type 2 diabetes is a chronic illness that is managed with a specific goal – reducing the complications of the disease. Diabetes can lead to cardiovascular disease (e.g., heart attacks), cerebrovascular disease (e.g., strokes), eye disease causing blindness, kidney disease leading to kidney failure and dialysis, and nerve disease leading to problems like foot ulcers that can eventually lead to amputations. The risks of these outcomes are reduced by managing blood sugar levels. Evidence shows that those with diabetes can have fewer complications if they can control blood sugars effectively. (How intensely blood sugar must be managed is a continued source of debate.)
Type 2 diabetes mellitus was once called adult-onset diabetes, typically affecting individuals older than 40 years.  Now, because the epidemic of obesity and inactivity in children, type 2 diabetes is occurring at younger and younger ages: it has been diagnosed in children as young as 2 years of age who have a family history of diabetes. Type 2 diabetes is characterised by peripheral insulin resistance with an insulin-secretory defect that varies in severity. 
For type 2 diabetes to develop, insulin resistance and delayed insulin production from the pancreas occurs. All overweight individuals have some degree of peripheral insulin resistance, but diabetes develops after the progression from normal glucose tolerance to abnormal glucose tolerance. Postprandial glucose levels gradually damage the beta cells of the pancreas. A powerful fore-runner to the type 2 diabetes is evidence of early pancreatic beta cell damage in reactive hypoglycaemia (for more information, please refer to Hypoglycaemia protocol). Reactive hypoglycaemia occurs as excessive fatty acids and glucose damage insulin secreting beta-cells and cause early-phase insulin release failure after eating. Despite having elevated blood sugars, the patient feels tired and hungry immediately after eating. This is followed by an over-compensation of late-phase insulin production, which causes a true hypoglycaemia, causing powerful hunger and fatigue, to continue the cycle.

If patients with reactive hypoglycaemia and insulin resistance remain untreated with dietary and lifestyle intervention, they will commonly progress to more severe pancreatic dysfunction and diabetes. These patients tend to exhibit the signs and symptoms of hypoglycaemia (low blood sugar), despite having elevated blood sugars of 4.5 to 6.0, or even above. Progression to more severe metabolic dysfunction and diabetes, the profound lack of energy occurs due to a blockade in mitochondrial energy production induced by excessive energy consumption, with elevated free fatty acids and hyperglycaemia, rather than lack of glucose.
Unfortunately, this lack of cellular energy production creates a strong unconscious drive to seek out energy dense foods and to conserve energy (to be sedentary) in an attempt to increase cellular energy, despite having a conscious desire to lose weight and get fitter.

Approximately 90 percent of patients who develop type 2 diabetes are obese.  Because patients with type 2 diabetes retain some ability to secrete endogenous insulin, those who are taking insulin do not develop diabetic ketoacidosis (DKA) if they stop taking it for some reason.  Therefore, they are considered to require insulin but not to depend on insulin.  Moreover, patients with type 2 diabetes often do not need treatment with oral anti-diabetic medication or insulin if they lose weight.

Aetiology / Risk factors
Major causative factors and risk factors that can contribute to the incidence of metabolic dysfunction include the following:

  • High calorie diet, high glycaemic load diet
  • Lack of exercise
  • Chronic stress
  • Digestive dysbiosis causing low-grade gut derived inflammation
  • Environmental toxicity
  • Hormonal imbalances
  • Chronic inflammation

Clinical indicators of type 2 diabetes include:

  • Hypertension
  • Vascular disease
  • Angina
  • Previous heart attack/stroke
  • Intermittent claudication


  • Acne
  • Skin tags (cutaneous papillomas, acrochordon)
  • Skin cancers
  • Male pattern (vertex) balding
  • Acanthosis nigricans

Reproductive (Female):

  • Early puberty
  • Amenorrhoea
  • Oligomenorrhoea
  • Polycystic ovarian syndrome
  • Infertility
  • Low SHBG


  • High calorie and carbohydrate cravings

  • Overweight
  • Weight accumulates over the stomach
  • History of failed weight loss attempts
  • Diabetes


  • Sleep apnoea
  • Snoring
  • Day time fatigue/sleepiness

Reproductive (Male):

  • Erectile dysfunction
  • Impotence
  • Prostate cancer


  • Depression
  • Tinnitus
  • Migraines
  • Headaches/Dizziness
  • Myopia (short-sightedness)

Diet and Lifestyle
Dietary and lifestyle guidelines may assist in the management of type 2 diabetes include:

  • Weight reduction where appropriate is essential. The Shake It Practitioner Weight Management Program is a safe fat loss program that sensitises insulin signalling, burns fat and helps to lower blood triglycerides and support healthy cholesterol levels.
  • For normal weight individuals, the diet should ideally be managed around regular blood sugar monitoring, and insulin intake. Following the principles of a balanced healthy regime to include at least 5 servings of vegetables, quality protein, reducing high glycaemic load foods, and to consume essential fatty acids (via nuts, seeds and fish) are all detailed in the Wellness and Healthy Ageing Program.
  • The Mediterranean Diet has been found to be beneficial in managing dyslipidaemia. This is comprised of whole grains, fresh fruits and vegetables, fish, olive oil and garlic. This diet is high in monounsaturated fatty acids and has been shown to increase HDL cholesterol plasma levels and reduce susceptibility to LDL oxidation. The principals of this diet are found in the Wellness and Healthy Ageing Program.
  • Lifestyle modifications that are beneficial include increased physical activity, stress reduction and smoking cessation.

Gestational Diabetes Mellitus

Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy.  Untreated GDM can lead to foetal macrosomia (big baby syndrome), hyperglycaemia, hypocalcaemia, and hyperbilirubinaemia.  In addition, mothers with GDM have increased rates of caesarean delivery and chronic hypertension. 

Normalisation of glucose levels in women with gestational diabetes will reduce the risk of complications such as macrosomia, birth trauma, need for caesarean section, and neonatal hypoglycaemia.  If dietary modification fails to improve glucose values, insulin therapy is indicated.  Oral hypoglycaemic agents are contraindicated during pregnancy.  Subsequent pregnancies can be affected, and the risk of developing type 2 diabetes is increased.  If maternal glucose levels are uncontrolled, the infant can suffer CNS defects, macrosomia, organomegaly, cardiac or renal anomalies, situs inversus (position of organs to reversed or mirrored), asphyxia, respiratory distress, increased blood volume, increased blood viscosity, congestive heart failure, hypocalcaemia, hypomagnesaemia, hypoglycaemia, or hyperbilirubinaemia, or the child may be stillborn. Abnormal maternal glucose regulation occurs in 3-10% of pregnancies, with the prevalence of diabetes among women of childbearing age increasing in the Western countries. 

Aetiology / Risk factors

  • Family history of type 2 diabetes:  having a first-degree relative with type 2 diabetes leads to lifetime risk of 40%; similarly 25% to 33% of all type 2 diabetics have a family history of the condition.
  • Age older than 40 years
  • Excess body fat, particularly truncal obesity with waist circumference >88 cm
  • Sedentary lifestyle with diet high in fats and calories
  • Glucose intolerance, dyslipidaemia, hypertension
  • History of gestational diabetes
  • History of polycystic ovarian syndrome
  • Aboriginal or Torres Strait Islander, Pacific Islander, Indian or Chinese, African American, Hispanic American, and Native American descent.
  • Low birth weight and/or malnutrition in pregnancy may cause metabolic abnormalities in a foetus that later lead to diabetes.

Signs and Symptoms

  • GDM only occurs during pregnancy.  The diagnosis is established by glucose tolerance testing.  The best method for diagnosing GDM continues to be controversial.  The 2-step system is currently recommended in the United States. A 50g, 1-hour screening test is administered to all pregnant women at 26-28 weeks’, followed by a 100g, 3-hour OGTT for those with an abnormal screening result.  Alternatively, a 1-step, 75-g, 2-hour test can be administered.  Other measurements (e.g., maternal HbA1C, random postprandial or fasting blood sugar level, fructosamine level) are not recommended because of low sensitivity.
  • Oral Glucose Tolerance Test prerequisites for gestational diabetes are as follows:
    • One-hour, 50g glucose challenge result greater than 7.8 mmol/L
      • Overnight fast of 8-14 hours
      • Carbohydrate loading for 3 days (>150 g carbohydrates)
      • Seated and not smoking during the test
      • Two or more values met or exceeded
      • Either a 2-hour (75 g of glucose) or 3-hour (100 g of glucose) test

Diet and Lifestyle

  • Goals during pregnancy should be to manage blood sugar levels and prevent excessive weight gain in the mother or baby, whilst still providing a range of essential nutrients.
  • Refined carbohydrates including sugar, sweets, fruit juices, white breads, pasta and potatoes should be avoided.  These foods have a high glycaemic index and are damaging in any amount for diabetics.
  • A diet high in fresh fruit (whole), vegetables (non-starchy), essential fatty acids and lean protein sources provides essential phytonutrients, antioxidants, magnesium and helps to control inflammatory processes in the blood vessels.
  • Smoking cessation is the highest priority in currently smoking patients.
  • Regular aerobic exercise has been shown to stimulate non-insulin dependent glucose transport into cells.