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BOTANICAL

CONSENSUS STATEMENT
Type II Diabetes Mellitus

1. Pathophysiology of Type II Diabetes Mellitus


Type II Diabetes Mellitus has historically been known as adult onset diabetes,
however it is more frequently being diagnosed in children and teenagers, and
it is becoming an epidemic. It is a multi-factorial condition and there are a
combination of causes involved including genetics, and environmental factors
such as overeating and lack of exercise leading to obesity, stress, and aging.
It is characterised by elevated glucose levels (hyperglycaemia) due to
impaired glucose metabolism as a result of a loss of cell sensitivity to insulin.
There is impaired regulation of hepatic glucose production with declining
function of pancreatic beta cells, and as the condition processes the beta
cells fail, insulin levels drop and this amplifies the effects of insulin resistance.
For Type 2 Diabetes to occur, insulin resistance and inadequate insulin
secretion must both exist (Hechtman 2014; Kahn et al, 2014; Mahler et al,
1999).

Many patients are asymptomatic, with the classic symptoms including


polyuria, polydipsia, polyphagia, and weight loss. Blurred vision and lower-
extremely paresthesias may occur in patients with progressed disease, as
well as fatigue, poor wound healing, periodontal disease and frequent
infections. Acute complications include hypoglycaemia, diabetic ketoacidosis
and non-ketotic hyperosmolar hyperglycaemia. Chronic complications include
cardiovascular diseases, cognitive decline, increased incidence of immune
dysfunction and autoimmune disease, depression, chronic pain,
hypercholesterolaemia, renal disease, retinopathy, cataracts, periodontal
disease and more (Hechtman, 2014; Medscape, 2018).

Medically, the condition is treated with diet and exercise, hypoglycaemic


medication and sometimes insulin injection.

2. Biomedical risk factors of Type II Diabetes Mellitus


o Age > 45
o > Waist to hip ratio
o Overweight / obesity
o > Fasting insulin levels
o Impaired fasting glucose or impaired glucose tolerance
o Family history (a parent or sibling with diabetes or hypoglycaemia)
o History of CVD (or family history of CVD)
o Hypertension
o Low LDL and/or triglycerides
o PCOS
o Identical twins
o Overweight / obese individuals at high risk due to insulin resistance
o Various genetic SNP’s have been associated with beta cell function
and insulin resistance
o Race – higher incidence in African American, Hispanic American,
Native American/Canadian, Native Australian or New Zealander,
Asian American, Pacific Islander
(Hechtman, 2014)

3. Holistic risk factors


o Food intake – nutritional excess; high intake of sugar, refined
carbohydrates, trans fats and low intake of fibre, antioxidants
o Nutrient deficiency
o Sedentary lifestyle
o High stress
o Depression
o Toxin exposure
o Socioeconomic status

4. Diagnosis of Type II Diabetes Mellitus


Type II Diabetes Mellitus diagnosis involves a fasting blood glucose test (10-
16hrs fast) with a resulting glucose concentration equal to or greater than
7mmol/L on at least two separate occasions.

A random blood glucose level equal to or greater than 11mmol/L with


symptoms such as polyuria, polydipsia, polyphagia, fatigue, blurred vision,
poor wound healing, periodontal disease and frequent infections is suggestive
of Type II Diabetes and further testing is warranted.

A glucose tolerance test consists of oral administration of 75g of glucose to


find out how fast it is cleared from blood, and it is used to assess for diabetes,
insulin resistance and reactive hypoglycaemia. A resulting venous plasma
glucose concentration equal to or greater than 11mmol/L at 2hrs after
ingestion, and at least one other sample during the 2hr test is indicative. A
fasting blood glucose test however, is more accurate and convenient.

A glycosylated haemoglobin test (HbA1c) is used to measure average blood


glucose control over the previous 2 – 4 months and it identifies what the
relative glucose load on the system has been by measurement of glycated
haemoglobin in blood. A result of <6-7% is optimal, 7-8% is mild, 8-9% is
moderate, >9% is severe. A result of >/=6.5% is required for a diagnosis of
DM. This test, combined with a fasting blood glucose test is the most
accurate way to diagnose Type II Diabetes Mellitus.

5. Conventional medical management of Type II Diabetes Mellitus


Not all patients diagnosed with Type II Diabetes Mellitus require medication,
and prescription is dependant on disease status and progression. Patients
need to work with their GP to monitor their condition, and take their
prescribed medications accordingly.

Medications that may be prescribed in this condition include:


• Biguanides – block glucose release from liver, slow glucose release
from gut, improves insulin sensitivity
• Sulphonylureas – stimulates pancreas to release more insulin
• DPP-4 inhibitors – blocks action of DPP-4 enzyme, stimulates release
of insulin, blocks release of glucose from liver
• SGLT2 inhibitors – blocks glucose from being reabsorbed by kidneys
• Thiazolidinediones - improves sensitivity of cells to insulin, decreases
glucose release from liver
• Alpha glucosidase inhibitors – slows digestion of carbohydrates from
food
• GLP-1 agonists – block glucose release from liver, slows glucose
release from gut, stimulates release of insulin
• Insulin – allows glucose to move from bloodstream to body cells
(The National Diabetes Services Scheme, 2016)
6. Botanical management of Type II Diabetes Mellitus
o Desired Objectives
- Support the pancreas to improve/restore function of beta cells
- Reduce resistance to insulin and improve glycaemic control
- Regulate and lower blood glucose levels
- Support liver to reduce inflammation, regulate glucose
production and protect against toxic damage
- Support nervous system to improve stress response
- Reduce weight to prevent long term complications
o Classes of medicines
! Anti-diabetic to alleviate the effects of diabetes
! Pancreatic Trophorestorative to heal and restore the pancreas
! Adaptogen to support cortisol release and reduce the destabilising
effects of high cortisol secretion on blood sugar, and improve
stress response
! Tonic to support and nourish the body
! Anti-obesity to assist in the reduction of body weight
! Hypoglycaemic to reduce level of glucose in the blood
! Anti-inflammatory to reduce inflammation
! Hepatoprotective to protect the liver against toxic damage
! Anti-oxidant to protect against oxidation and free radical damage
(Bone, 2007; Bone & Mills, 2013; Hechtman, 2014)
o Specific medicines
Herb Actions Weekly Justification
Dosage
Nigella Anti-diabetic, anti- 30-80ml Improves glucose tolerance and antioxidant
sativa inflammatory, anti-oxidant, 1:2 LE status, decreases blood glucose, serum
hepato-protective (Ahmad (Mediherb, insulin and glycated haemoglobin levels
et al, 2013; Braun & Cohen, 2015) (Braun & Cohen, 2015). Kaatabi et al (2015)
2015; Mediherb, 2015) found that long-term supplementation in
conjunction with standard Type 2 DM oral
hypoglycaemic drugs improves glucose
homeostasis and enhances antioxidant
defence system. Shaafi & Kulkarni (2017)
found Nigella sativa significantly lowered
fasting blood glucose, postprandial blood
Herb Actions Weekly Justification
Dosage
glucose and glycosylated haemoglobin after
8 weeks in patients with poor glycaemic
control on conventional medication. A meta-
analysis by Daryabeygi-Khotbehsara et al
(2017) found Nigella sativa significantly
improves fasting blood sugar, and states that
current findings suggest supplementation is a
suitable choice for managing the
complications of Type 2 DM.
Cinnamo Anti-diabetic (Bone, 2007; 10-30ml Reduces fasting blood glucose and improves
mum Braun & Cohen, 2015) 1:2 LE insulin sensitivity (Braun & Cohen, 2015;
cassia (Bone, 2007) Hechtman, 2014). A meta-analysis by Allen
et al (2013) found that cinnamon doses of
120 mg/d to 6 g/d for 4 to 18 weeks reduced
levels of fasting plasma glucose, but that no
significant effect on glycosylated
haemoglobin was seen.
Gymnema Anti-diabetic, 25-75ml Reduces intestinal absorption of glucose,
sylvestre hypoglycaemic, pancreatic 1:1 LE inhibits glucose transport in small intestine,
trophorestorative (Bone, (Bone, 2007) increases number of cells in pancreas
2007, Braun & Cohen, responsible for insulin production,
2015) regenerates beta cells and improves insulin
secretion, improves fasting blood glucose
and glycosylated haemoglobin levels
(Alternative Medicine Review, 1999;
Hechtman, 2014; Tiwari et al, 2014). Devi &
Jain (2015) concluded that Gymnema
sylvestre gymnemic acid neutralises sweet
taste receptors, which in turn curbs sugar
cravings and could help control caloric intake
and thus be useful I control of diabetes and
obesity. A systematic review by Leach (2007)
concluded Gymnema sylvestre targets
chronic inflammation, obesity, enzymatic
Herb Actions Weekly Justification
Dosage
defects, and pancreatic cell function, and as
such may be useful in management of
diabetes and prevention of the associated
pathological changes (however efficacy has
only been supported by a small number of
non-randomized open-label trials).
Panax Adaptogen, tonic, 7-40ml Improves resistance to chronic stress,
gingeng hypoglycaemic, anti- 1:2 LE reduces inflammation by inhibition of NF-
inflammatory (Bone, 2007) kappaB, lowers blood glucose, improves
(Bone, 2007; Braun & pancreatic beta cell function (Braun & Cohen,
Cohen, 2015; Hechtman, 2015; Hechtman, 2014; Panax Ginseng,
2014) 2009). A study by Luo et al (2016) found that
ginsenosides (which are contained in Panax
ginseng) have a positive effect on pancreatic
beta cell function. In particular Rb2 increases
islet beta cell insulin release and promotes
beta cell migration, and Re has some impact
on cell migration. A systematic review by
Shergis et al (2012) states that the results
from the studies included gave some
indication that Panax ginseng has a positive
effect on overall glycaemic response and
ability to lower circulating glucose.
Trigonella Hypoglycaemic, anti- 15-30ml Reduces intestinal absorption of glucose,
foenum- inflammatory (Bone, 2007; 1:2 LE improves peripheral glucose utilisation,
graecum Braun & Cohen, 2015) (Bone, 2007) improves fasting blood glucose values,
(Braun & Cohen, 2015; Hechtman, 2014). A
meta-analysis by Neelakantan et al (2014)
found that clinical trial results support
beneficial effects of Trigonella foenum-
graecum on glycaemic control in persons with
diabetes. Gupta et al (2001) found that
Trigonella foenum-graecum improves
glycaemic control and decreases insulin
Herb Actions Weekly Justification
Dosage
resistance in mild Type II Diabetes.
Silybum Hepatoprotective, 30-60ml Decreases oxidative stress, inhibits
marianum antioxidant (Bone, 2007; 1:1 LE production or release of pro-inflammatory
Bone & Mills, 2013; Braun (Bone, 2007) mediators, inhibits NK-kappaB and
& Cohen, 2015) suppresses TNF-alpha and iNOS, reduces
formation of beta amyloid deposits which
contribute to beta cells dysfunction and
enhances viability of pancreatic beta cells,
reduces metabolic pathways that contribute
to glycaemia maintenance (i.e.
gluconeogenesis in fasted state and
glycogenolysis and glycolysis in the fed state)
supporting its antihyperglycaemic effect
(Braun & Cohen, 2015). Huseini et al (2006)
found that silymarin significantly decreased
HbA1c, FBS, total cholesterol, LDL,
triglyceride SGOT and SGPT levels
compared with placebo after 4 months. A
review by Stolf et al (2017) concluded that
silymarin is capable of attenuating common
diabetic complications in several organs,
including nephropathy, neuropathy, impaired
healing, retinopathy, hepatopathy, metabolic
disorders, and cardiomyopathy.

o Non-pharmacological treatments
- Counselling (nutritional and psychological)
- Stress management / reduction – yoga, meditation
- Regular exercise routine to improve insulin sensitivity and
reduce weight and cardiovascular risk
- Adherence to low GI and GL diet and appropriate caloric intake
- Polyphenol rich diet (Bahadoran et al, 2014)
- Chromium Picolinate 200-1000mcg/day: facilitates glucose
uptake into the cell (Hechtman, 2014)
- Magnesium 400mg/day – deficiency is linked to poor
glycaemic control and impaired insulin secretion. Insulin
resistance can interfere with cellular uptake of magnesium
causing a vicious cycle (Hechtman, 2014)
- Alpha lipoic acid: antioxidant which regenerates other
antioxidants like Vitamin C, E, glutathione and CoQ10, and
enhances glucose uptake (Braun & Cohen, 2015; Hechtman,
2014)

7. Recommendations for the future: how botanical medicines may be


integrated into a combined care plan
Herbal medicines alongside lifestyle and pharmaceutical interventions are
proven to be a valuable adjunct in a combined care plan. Specific classes of
herbal medicines are able to effectively meet treatment objectives in Type II
Diabetes Mellitus via the synergistic effects of their constituents, which have
been shown to have positive effects on the variety of morbidities associated
with this condition such as blood sugar dysregulation, defective pancreatic
beta cell function, insulin resistance, chronic inflammation, micro and macro
vascular disease, obesity and more.

Whilst appropriate nutritional intake and regular exercise are essential in


management of T2DM, herbal medicine is able to offer a great deal in the
treatment of this chronic disease, even reducing or removing the need for
pharmaceutical medications. Mechanisms such as inhibition of carbohydrate
absorption in the intestine, protecting pancreatic beta cell function, improving
insulin sensitivity and stimulating insulin secretion are all useful in the
treatment and management of this condition.

Due to their blood sugar lowering effects Nigella sativa, Cinnamomum cassia,
Panax ginseng, Trigonella foenum-graecum, Silybum marianum and
Gymnema sylvestre may have additive effects in patients on anti-diabetic
drugs such as Biguanides, Sulphonylureas, DPP-4 inhibitors, SGLT2
inhibitors, Thiazolidinediones, Alpha glucosidase inhibitors, GLP-1 agonists
and Insulin, therefore they should closely monitor their blood sugar levels and
work with their doctor to adjust medication accordingly.
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