metabolic balance® and Diabetes
© Dr. Wolf Funfack, MD, Specialist in Internal Medicine/Nutritional Medicine
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© metabolic balance GmbH
Diabetes worldwide
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Diabetes worldwide
Update 2012
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Data from the Canadian Diabetes Association
Prevalence of diabetes in Ontario adults >35 years
year
cases
population
Prevalence rate
1995
341.893
5 269.107
6,49%
2000
495.134
5 996.214
8,26%
2005
707.196
6 709.338
10,54%
WHO: Until 2030 an increase of 40% is estimated for Canada!
(Canadian Journal of Diabetes 2009;33(1):35-45)
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BMI and its sequelae
Type 2 diabetes
High blood pressure
Gall stones Heart disease
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From: Nature, special issue - Diabetes, 2001
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Waist measurement as a risk factor
Risk of developing diabetes
Waist circumference
in men
in women
Low risk
<
94 cm (37)
< 80 cm (31,5 inches)
Slightly increased risk
>
94 cm
> 80 cm
Significantly increased risk
>
102 cm (40)
> 88 cm (34,65 inches)
Average waist circumference e.g. in Germany:
Women = 89 cm men = 98 cm
The risk of diabetes is halved with a weight loss of only 4 kg.
Other risk factor: high levels of triglycerides.
From: German Health Report Diabetes 2008
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Reduced life expectancy due to diabetes
Age at the time of diagnosis
In years
20 to <30
15 to 20
30 to <40
10 to 13
Over 65
2 to 5
Life expectancy in Germany
Women: 83 years
Men:
78 years
Source: Health Report, German Federal Ministry of Health 2006
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Increased risk of long term complications
due to diabetes
Disease
Circulatory disorders
- affecting the heart
- affecting the limbs
Risk of disease for diabetics
15 - 20
2-6
20 - 35
Stroke
2-3
Blindness
10 - 25
Chronic kidney failure
15 - 20
The average risk of disease in the population is 1
Source: Health Report, German Federal Ministry of Health 2006
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The costs of diabetes in Europe
Stroke:
every 12 minutes
Heart attack/amputation:
every 19 minutes
Dialysis dependence:
every 60 minutes
Blindness caused by diabetes:
every 90 minutes
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Liebl et al DMW 2001;126 : 585-89 CODE-2 Study (Costs of Diabetes in Europe)
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Blood sugar regulation
High
blood sugar
Pancreas
Insulin release
Glucose uptake
from fat and muscle cells
Normal
blood sugar level
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Blood sugar regulation
Low
blood sugar
High
blood sugar
Pancreas
Glucagon release
Glucose release
by the liver
Insulin release
Glucose uptake
from fat and muscle cells
Normal
blood sugar level
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How does
glucose reach the cell?
Glucose
Glucose
Glucose
Glucose
Glucose transporter
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Muscle contraction
and glucose transporters
Muscle contraction has the same effect as insulin!
Glucose
Glucose
Glucose
Glucose
Muscle contraction
Glucose transporter
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Blood sugar and serum insulin during i.v. glucose tolerance test
in 8 test subjects of normal weight and 10 obese subjects
Source: from Karam, J.H. et al. 1963
Blood- 450
sugar
400
(mg%)
350
Serum- 180
insulin
(µE/ml) 160
140
300
120
Obese
250
100
200
80
150
60
100
40
50
Normal weight persons
0
Obese
Obese
Normal weight
weight persons
persons
Normal
20
0
0
15
30
45
60
75
Minutes
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90 105 120
0
15
30
45
60
Minutes
75
90 105 120
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Obesity and the metabolic syndrome
493 children + adolescents
(age 4 - 20) exclusion:
medication to treat
hypertension, diabetes or lipids
Normal weight
Overweight
Slight obesity
Severe obesity
Age (years)
11.7
11.9
12.8
11.3
MBI
18.4
24.5
33.4
40.6
Glucose (mg %)
87.4
86.8
89.6
89
Insulin (µU/ml)
10.3
14.6
31.3
38.6
Triglyceride (mg %)
48.4
83.1
104.6
96.5
HDL-Chol. (mg %)
58.5
46.7
41.1
39.9
CRP (mg %)
0.01
0.05
0.13
0.33 15
(Source: R. Weiss, NEJM, June 3, 2004; 350: 2362-74)
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Insulinresistance and muscles
Muscle cells do not store fat anymore
and release it to the blood!
Fat is transported into the liver!
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Insulinresistance and the liver
Fat is stored in the liver cells!
They do not react on insulin anymore,
so the release of glucose is not blocked!
Fat from the liver is transported into the
a- and b-cells of the pancreas.
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Insulinresistance and the pancreas
Insulinresistant a-Cells
produce more Glucagon!
Insulinresistant b-Cells
produce more Insulin!
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Insulinresistance and the brain
Insulinresistant cells of the brain
cause stressreactions!
In situations of stress
the liver releases Glucose!
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Insulinresistance and the kidneys
In Insulinresistance
The kidney increases the Glucose levels by:
1. Gluconeogenesis
2. Increased Glucose Reabsorption
Gluoneogenesis in the kidney can
Increase by 300%!!
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Fructose leads to
faster fat storage
Fructose
Glucose
Not insulin dependent
Insulin dependent
No storage
Metabolism
Storage form
Fatty liver disease!
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Reduction in Body Weight
62,5 %
50 %
of participants need to
reduce their weight by
more than 5% and need
to maintain it for more
than one year.
of participatns reduced their
weight by more than 5%
and maintained it at least
for one year.
metabolic balance®
International recommendations for long-term
success of an efficient weigh management program
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Comparison of weight reduction programs
31,0%
21,0%
26,0%
21,0%
15,7%
14,3%
17,0%
62,5%
Weight watchers
Slimming world
Rosemary Conley
NHS Size Down
General Practice
Pharmacy
Exercise comparator
metabolic balance®
50%
Jolly, Kate et al. BMJ, 2011, 343; d6.500
“Comparison of range of commercial or primary care led weight reduction programmes . randomised controlled trial”
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Results of the
evaluation study insulin requirements)
8.30%
Before the study
8,3% of the participants were treated with insulin
End of the study
3,9% were still on insulin
3.90%
53 % of diabetics could stop their
insulin even after 1 year.
Before
Beginn
der Studie
Ende End
der Studie
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Case history
Mr G. L. a 47 year old teacher, with Type 2 diabetes, hypertension and
impaired lipometabolism
Medication:
Depot insulin:
morning 32 I.U., evening 16 I.U.
short-acting insulin: 3x a day before meals depending on blood sugar values
between12 and 18 I.U. daily insulin dose 70 - 90 I.U.
Hypertension:
80 mg Metoprolol, 10 mg Amlodipin, 16 mg Valsartan,
Other drugs:
40 mg Simvastatin, 100 mg aspirin
Omeprazol 20 mg if required for stomach ache.
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Case history
After 2 weeks:
Weight loss 8.4 kg,
depot insulin:
only 1 x 12 I.U. before meals;
short-acting insulin: between 8 and 12 I.U.
other medication:
20 mg Metoprolol, 8 mg Valsartan,
Amlodipin and Simvastatin were discontinued.
It was no longer necessary to take Omeprazol at this stage.
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Case history
In the 4th week:
Weight loss has plateaued,
frequent low sugar and hunger pangs during the day.
He has been exercising more in the last week,
e.g. Nordic walking and 1 day in the gym.
Fasting blood sugar was higher in the morning than in the evening
even if he did not eat anything in the night.
After this, depot insulin was discontinued
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Case history
Comparison of values at the start and end
Initial weight:
127.0 kg
BMI: 40,1
Final weight:
86.4 kg
BMI: 27.3
Height: 1.78 m
All medications were discontinued
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Case history
BP
HR
Chol.
LDL
HDL
Trigl.
HBA1c
LDL/HDL
02.04.2008
166/110
88/min
278
183
39
264
7.6
4.7
25.08.2008
125/80
72/min
167
119
53
134
6.2
2.2
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Source: http://www.evolvehealth.nl/mental-coaching/
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Canada: 1-289-291-3959
Many thanks
for
your attention!
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