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Metabolic Disease
Dr. Alta Smit
Canada
April 2004
Metabolic Disease
Disorders of fat and sugar metabolism
Obesity
Metabolic syndrome
Diabetes Type I and Type II
Disorders of calcium metabolism
Osteopenia
OBESITY
Modern Epidemic
Disorders of Fat and
Sugar Metabolism
Modern evidence to substantiate the
six-phase table of disease
Homotoxicology
Humoral Phases Matrix Phases Cellular Phases
Excretion Inflammation Deposition Impregnation Degeneration Dedifferention
phase phase
phase phase phase phase
Ectodermal
Endo-
dermal No enzyme damage Enzyme damage
Mesen-
chymal
Excretion principle Compensation principle
Meso- Natural healing Chronic Diseases
dermal tendency
Tissue
Biological division
Dedifferen-
Excretion Reaction Deposition Impregnation Degeneration tiation
Central
Reactive obesity
Metabolic Colorectal
Hypogly- Diabetes
syndrome Cancer
cemia Mellitus
Type II
Breast
NASH Osteoporosis
syndrome Myeloma
Pancreas
CA
Measurement of Obesity
Degree of
Body mass index (BMI) overweight/obesity-measures
body fat and muscle mass
Waist hip ratio (WHR) Abdominal fat in relation to
body size
Sagittal abdominal diameter Fat in the abdomen
Waist measurement Fat in and around the
abdomen
WHO’s Definition of Obesity
BMI (body mass index)
Weight (kg) is divided by
height (m2 )
E.g. Individual which weighs 90 kg and is 170 cm tall:
90 kg
= BMI 31
1.70 m x 1.70 m
kg = 2.2 pounds
m = 3.3 feet
WHO’s Definition of Obesity (BMI)
Normal weight 18.5- 24.9
Overweight 25-29.9
Obesity Grade I 30-34.9
Obesity Grade II 35-39.4
Obesity Grade III 40-
WHO’s Definition of Obesity
Upper limits for waist-hip ratio (WHR) and waist
circumference
Upper limits Male Female
Waist hip ratio (WHR) >1.0 >0.85
Waist circumference
94 cm 80 cm
(increased risk)
102 cm 88cm
Waist circumference
(greatly increased risk)
OBESITY
IS IT A CHRONIC RELAPSING
NEUROCHEMICAL DISEASE?
Neurochemistry of Appetite
Fat tissue and
Stomach
pancreas facilitate
secretes
the secretion of
Ghrelin
Insulin and Leptin
appetite
appetite
Source: Cummings DE, Schwartz MW. Genetics and Pathophysiology of human obesity.
Annu. Rev. Med. 2003; 54: 453-71
Ghrelin
Ghrelin
Recently discovered
Secreted primarily by the stomach
Interacts with neurons in the hypothalamus
Powerfully increases short term food intake
May decrease energy expenditure and fat catabolism
Also increases body weight by other mechanisms than
stimulating appetite
Hormonal Effects of Leptins
Inhibits the secretion of:
Cortisol
Aldosterone
DHEA
Reduce the secretion of catecholamines (adrenalin
and noradrenalin)
Obesity
Both leptins and insulin are increased in obese
individuals, but the cells are resistant to it
Fat Tissue (more than just a filler)
Metabolic organ
Hormonal organ
Immune organ
Fat Tissue as a Metabolic Organ
Secretes substances called adipocytokines
These have profound metabolic and
immunological consequences
White adipocyte (Fat Cell)
Fat Tissue as a Metabolic Organ
Adipocytokines
Adiponectin
TNFα
White adipocyte
NEFA
IL-6
Resistin
Leptin
TNF= tumor necrosis factor
Source: Fasshauer M, Paschke R.
IL-6= interleukin 6 Regulation of adipocytokines and Insulin resistance.
NEFA= non esterified fatty acids Diabetologia 2003; 46:1594-1603
Effects of the Adipocytokines
IL-6: Insulin resistance,
pro-inflammatory cytokine
TNFα: Increased in obesity,
modulates insulin sensitivity
Adiponectin: Important insulin sensitizer
Leptin: Major (down) regulator of food intake
and appetite
Resistin: Modulates insulin sensitivity
Fat Tissue
Gives rise to insulin resistance and
the Metabolic Syndrome
Effects of adipocytokines on insulin sensitivity
adrenergic agonists
Insulin
TNFα
IL-6
Adiponectin
Non esterified fatty acids
NEFA
Insulin
Source: Fasshauer M, Paschke R.
Regulation of adipocytokines and Insulin resistance. Resistance
Diabetologia 2003; 46:1594-1603
Obesity as an Immune
Syndrome
Obesity is an inflammatory state and
gives rise to tissue destruction and eventually
cancer
Fat Tissue as an Immune Organ
TGFβ
INTERLEUKIN 1 Adipocyte
TNF TH3 and other
IL-6 cells
TISSUE INFLAMMATION TISSUE REPAIR
AND DEGRADATION (free radicals)
Atherosclerosis
Tissue healing
Cancer
Inflammation: Cytokines
Cause inflammation Stop inflammation
Degrade tissues Tissue repair
Interleukin 1 Interleukin-10
Interleukin-6 Transforming growth
Interleukin-8 factor β
Tumor necrosis factor
From:
From: Th2 cells
Macrophages Th3 cells
Th1 cells From numerous cells in the
Chondrocytes
body
Fibroblasts
Local Mediators
Histamine
Serotonin
Preformed Lysosomal
Enzymes
granules
Prostaglandins
Free radicals
Nitric oxide
Cytokines
Newly
synthesized
Traumeel Down Regulates
TNFα and IL-6
Study at Weizmann Institute
Fat Tissue As A
Neuroendocrine Organ
Neuro endocrine interactions
Growth hormone
Eating centre
Insulin resistance
Cortisol and aldosterone
Secretes insulin
PCOS
Fat Tissue
Causes edema and high
blood pressure
Fat Tissue as an Endocrine Organ
Fat tissue increases the secretion of aldosterone
from the adrenal gland
Aldosterone (minerallocorticoid) causes water
retention and hypertension
Cortisol causes insulin resistance
Growth Hormone and Insulin growth factor-
1(IGF-1)
Fat Tissue
Gives rise to atherosclerosis and
free radical formation, and also
hypertension
Fat Tissue as a Promoter of Free
Radicals and Hypertension
Nitric oxide (NO) binds with the hydroxyradical
(OH) to form the highly dangerous free radical,
peroxynitrite.
NO is needed for vasodilatation (action on
smooth muscle). If it is decreased (obesity and
diabetics), hypertension ensues.
Metabolic Syndrome
20-25% of US adults have it
Metabolic Syndrome: Risk Factors
Central obesity
Atherogenic dyslipidemia (high triglycerides and
low HDL)
Raised blood pressure
Insulin resistance or glucose intolerance
Prothrombotic state
Pro-inflammatory state (elevated C-reactive
protein)
Metabolic Syndrome: Diagnosis ATP III
Criteria
Abdominal obesity
men >102 cm (40 in)
women >88 cm (35 in)
Triglyceride > 150 mg/dL (1.7 mmol/L)
HDL cholesterol
men <40 mg/dL (1.0 mmol/L)
women <50 mg/dL (1.3 mmol/L)
Blood pressure >130/>85 mm Hg
Fasting glucose >110 mg/dL (6.1 mmol/L)
Diagnosis of metabolic syndrome is made when 3
or more of the above risk determinants are present
STEATOTIC HEPATITIS (NASH)
Diabetes
Two types
Type 1
Results from an absolute deficiency of
insulin
Autoimmune destruction of the β-cells of
the pancreas
Genetically predisposed individuals (HLA-
type)
Initiated by a trigger (virus, chemical, etc.)
Diabetes
Type II
Much more prevalent, also now in
children (MODY= mature onset
diabetes of the young)
Results from inadequate insulin
response to demand
Due to insulin resistance and later
inadequate insulin
Diabetes: Diagnosis
Fasting blood sugar (FBG) test is the preferred
method
Fasting overnight (at least 8 hrs)
FBG of 100 mg/dL (5.5 mmol/L) is normal
IFG (Impaired fasting blood glucose)
110-126 mg/dL (6.1 – 7.0 mmol/L)
Diabetes
> 126 mg/dL (7.0 mmol/L) on two occasions = Diabetes
Random samples may be used if symptoms are
present
200 mg/dL (11.1 mmol/L) = Diabetes
Symptoms of Developed Diabetes
Polyuria (excessive urination)
Polydipsia (excessive thirst)
Weight loss
Blurred vision
Impairment of growth
Keto-acidosis
Long-Term Complications of Diabetes
Include:
Increase in atherosclerotic cardiovascular peripheral
vascular and cerebrovascular disease
Peripheral neuropathy with the risk of foot ulcers and
amputation
Retinopathy with potential loss of vision
Nephropathy leading to renal failure
Autonomic neuropathy causing gastrointestinal,
genitourinary, cardiovascular symptoms and sexual
dysfunction
Hypertension, Dyslipidaemia and Periodontal disease
Advanced Glycosylation End Products
(AGE)
AGE’s are immunogenic
(stimulate the inflammatory response)
Diabetics have an increase in IL-6, TNFα, and
free radicals, such as peroxynitrite (from NO
and OH)
Diabetics have less TGFβ, thus tissue repair is
decreased and inflammation is increased
Source: Matsomuro et al. Diabetes 2000; 49: 1711-1723
Matrix Structures
Cells:fibroblasts
Ground substance (proteoglycans and
glycosaminoglycans; PG/GAGs)
Three vascular structures
• Arteries
• Veins
• Lymph vessels Psycho-neuro-
Three neural structures endocrino-
• Sympathetic fibres immunology
• Parasympathetic fibres
• Sensovisceral fibres
Structure of the Matrix
Fibroblast
PAG’s
GAG’s
Fibroblasts and Tissue
TGFβ
INTERLEUKIN 1
TNF
IL-6 TH3cells
TISSUE INFLAMMATION TISSUE REPAIR
AND DEGRADATION (Free radicals)
Atherosclerosis
Tissue healing
Cancer
Diabetic Process in the Matrix
Hyperglycemia
Binding of
Auto- glucose aldehyde
oxidation Nonenzymatic group
glycosylation to proteins
Oxidative
Advanced glycation
stress end products (AGE)
Auto-
oxidation Oxidative stress
Reduction equivalents
decrease
Free radicals
increase
NFkB increases in
defensive cells
Inflammatory
cytokines increase
Matrix edema
Nonenzymatic
glycosylation
Development of AGE
Binding of
glucose aldehyde
group
to proteins Thickening of Thickening of
basal membrane anchor and radial fibres
Circulation disturbance Disturbed
Capillaries and perineurium lymph function
Colloidal osmotic
Edema in the pressure rises
nerve sheaths
Matrix edema
Homotoxicology
Humoral Phases Matrix phases Cellular Phases
Excretion Inflammation Deposition Impregnation Degeneration Dedifferention
phase phase
phase phase phase phase
Ectodermal
Endo-
dermal No enzyme damage Enzyme damage
Mesen-
chymal
Excretion principle Compensation principle
Meso- Natural healing Chronic Diseases
dermal tendency
Tissue
Biological division
Aim of Treatment
Treat the current condition
Treat the complications
Cardiovascular disease
Peripheral vascular disease
Renal disease
Ocular disease
Treat the cause and the imprint
Multicentric Approach
Classic
Homeopathic Remedy
Trace Element
Minerals
Amino acids
Mother tincture
Chinese Herbal Remedy
Essential oil
FIRE
Fear Of Rejection IMPREGNATION QUADRANT
Failure
AGING
INTOXICATION
PLETHORA
HYPERTENSION
POINTS: SI 16. HE 1
EARTH
METABOLIC QUADRANT
Lack of Nurturing
Seeking the mother
SYNDROME X
INSULIN RESISTANCE
ARTHEROSCLEROSIS
DYSLIPIDEMIA
GOUT
DIABETES
POINTS:ST20,SP8
WOOD
Liver: Toxic Quadrant
Decision making, planning,
Anger, frustration VIRAL INFECTIONS
TUPS IRRITABILITY, ANXIETY
STRESS
POINTS: Liv 1, GB 24, GB 20
Constitution Environmental Regulation failure Phase shift
imprint
Genetics
Ontogenesis
and primitive
imprints
B
i
o
l
o
g
Disease and i
organ system c
a
l
c
Phylogenesis u
t
Choice of treatment: On Phylogenesis
•Symptomatic
•Indication based
•Specific for that disease
Genetics B
And primitive
imprints
i
o
l
o
g
Disease and i
Organ system c
a
l
c
Phylogenesis u
t
Environmental Regulation failure Phase shift
imprint
Choice of treatment:
On Ontogenesis Ontogenesis
B
Phase i
Medications o
REGULATION
l
o
g
i
c
a
l
c
u
t
Treatment Plan on Six-Phase Table
Organ regulation and
Detoxification Cellular activation immunomodulation
ontogenesis
PPG’s MPG’s CPG’s ORPG’s
Phase remedies:
Phylo-
genesis
catalysts and tissue remedies
(compositum)
PPG’s MPG’S
Symptomatic and = basic remedies and
Functional support Homaccords
Three Pillars of Homotoxicology:
Treatment of the Metabolic Syndrome
CELLULAR ORGAN REGULATION
DETOXIFICATION AND IMMUNOMODULATION
ACTIVATION
HEPAR COMPOSITUM
LYPHOSOT GLYOXAL COMP FUNICULUS UMBICALIS
SUIS-INJEEL
UBICOENZYME PANKREAS SUIS-INJEEL
TRAUMEEL
CRALONIN
Traumeel (Drops)
D8
D6
D4
D3
D2
Hammamelis Belladonna Echinacea
Arnica Hepar sulf Hypericum Chamomilla
Angustofolia
Calendula Millefolium Aconitum Symphytum
officinale Bellis perrenis Echinacea purp
Ubicoenzyme (Drops)
D200
D30
D8
D4
D2
Beta Oxcalic NAD Succinic Hydrastis Silicea
Lipoic Calc Thuja Sulphur
Vulgaris acid Citrate acid
acid Carb
Glyoxal Compositum Ampoules
Methylglyoxalum D10
Glyoxalum D10
Galium-Heel
Betula alba’s leaves contain saponins, which
have diuretic properties.
D12
D10
D8
D6
D5
D4
D3
D2
Galium Semperv. Caltha Hedera Echinacea Acidum
aparine tectorum palustris Helix angust. nitr.
Conium Clematis Ononis Betula Calcium Argentum Symphytum
maculatum spinosa alba fluoratum officinale
Sedum Thuja Juniperus Saponaria Phosphorus Apis Urtica
Lifestyle Changes in Metabolic
Disease
Diet low in carbohydrate and saturated fat
Diet relatively rich in protein, especially organic
fish
Mediterranean diet
Measures to reduce insulin secretion, e.g. protein
before alcoholic drinks
Physical exercise
WEIGHT LOSS is the most important
Obesity
SYMPTOMATIC SEROL
Basic remedy
Homaccord
Graphites-Homaccord
+
Detoxification DETOX-KIT
SUPPORT
REGULATION Immunomodulation Traumeel
+
Cellular activation UBICOENZYME
INDUCE
VICARIATION Hypothalamus suis-Injeel
Phase or tissue
remedy
Glandula suprarenalis
suis-Injeel
Funiculus umbicalis suis-Injeel
Metabolic Syndrome
Traumeel
SYMPTOMATIC
Basic remedy Cralonin
Homaccord Lithiumeel (gout)
SEROL
REDUCHOL
+
DETOX-KIT
DETOXIFCATION
SUPPORT
FUNICULUS UMBICALIS
REGULATION IMMUNOMODULATION SUIS-INJEEL
+
CELLULAR ACTIVATION GLYOXAL COMPOSITUM
UBICOENZYME
INDUCE
VICARIATION PANKREAS SUIS-INJEEL
PHASE HYPOTHALAMUS SUIS-INJEEL
REMEDY GLANDULA SUPRARENALIS SUIS-
Or TISSUE REMEDY INJEEL
Diabetes Type II +
Treat complications
REDUCHOL
SYMPTOMATIC
SEROL
MAIN REMEDY Cralonin
SECONDARY Traumeel
REMEDY
Lithiumeel (gout)
+
DETOX-KIT
DETOXIFCATION
SUPPORT
FUNICULUS UMBICALIS
REGULATION IMMUNOMODULATION SUIS-INJEEL
+ CELLULAR ACTIVATION
GLYOXAL COMPOSITUM
INDUCE
VICARIATION PANKREAS SUIS-INJEEL
HYPOTHALAMUS SUIS-INJEEL
PHASE
GLANDULA SUPRARENALIS SUIS-
REMEDY AND INJEEL
TISSUE REMEDY
Diabetes Type I (Adjuvant Treatment)
SYMPTOMATIC
LEPTANDRA COMPOSITUM
BASIC REMEDY TRAUMEEL
+
DETOXIFICATION DETOX-KIT
SUPPORT
GALIUM-HEEL
REGULATION IMMUNOMODULATION
+ UBICOENZYME
CELLULAR ACTIVATION
GLYOXAL COMPOSITUM
INDUCE
VICARIATION PANKREAS SUIS-INJEEL
PHASE
REMEDY AND VISCUM ALBUM-INJEEL
TISSUE REMEDY
(insulin effect)
Regulation Pyramid
Immune
Neuro endocrine
Cellular
metabolism
Enterohepatic
matrix toxicity
Three Pillar Treatment of Obesity/Metabolic
Syndrome/Diabetes Type II
Weeks 1-12
Basic remedy and Homaccord remedy
10 drops/1 tablet
3x per day
Detox and organ activation
Nux vomica-Homaccord
Berberis-Homaccord
Lyphosot
Cellular activation
Glyoxal compositum
Ubicoenzyme (drops)
Organ regeneration
1 ampoule twice
Funiculus Umbicalis suis-Injeel
a week
Hypothalamus suis-Injeel
Ubicoenzyme
Glandula suprarenalis suis-Injeel
10 drops 3x per day
Pankreas suis-Injeel
Three Pillar Treatment of Diabetes Type I
Weeks 1-12
Basic remedy and Homaccord remedy 10 drops/1 tablet
3x per day
Detox and organ activation
Nux vomica-Homaccord
Berberis-Homaccord
Lyphosot
Cellular activation
Glyoxal compositum
Ubicoenzyme (drops)
Organ regeneration
1 ampoule twice
Pankreas suis-Injeel
a week
Viscum album-Injeel
Ubicoenzyme
10 drops 3x per day
Three Pillar Treatment of Obesity/Metabolic
Syndrome/Diabetes Type II
Weeks 12 and after
Basic remedy and Homaccord remedy
Detox and organ activation
10 drops/1 tablet
Lyphosot 3x per day
Cellular activation
Glyoxal compositum
Wait 6 weeks on this regime
to allow for vicariation, then repeat treatment for
weeks 1-12, wait again for vicariation, then repeat.
Normally a couple of cycles are needed until full vicariation
really occurs
Weight Control Program
Obesity
Treatment
SEROL
Hepar compositum
St 36
Lyphosot
SP 6
Weight Control Program
Endocrine classification
Hypophysis
Apple shaped
Thick trunk
Thin extremities
Treatment
Hypothalamus suis-Injeel
Glandula suprarenalis suis-Injeel
Glavella
ST 23, 25, 27
Weight Control Program
Endocrine classification
Pancreas
Pear shaped
Increased abdominal fat
Treatment
Pankreas suis-Injeel
Hepar compositum
Solar plexus
LR 13
ST 25, 36
Weight Control Program
Endocrine classification
Ovaries/Testicles
Lower extremity fat
Treatment
Hormeel
St 29
Sp 6
Treatment of Diabetic Complications
Cardiovascular disease (Cralonin)
Journal of Biomedical Therapy - Spring 2004
Antioxidant (also Ubichinon compositum)
Antihypertensive (also Rauwolfia compositum)
Coronary circulation (also Ateria-Heel and Cactus-Injeel)
Helps cardiac failure
Helps against hyperlipidemia (also add Barijodeel)
Peripheral circulation (also Aesculus compositum)
Polyneuropathy- Lyphosot/Lymphomyosot
Nephropathy- Equisetum arvense-Injeel
Microalbuminuria early sign
Ocular- Oculoheel
Treatment of peripheral diabetic
polyneuropathy (PNP) with
Lymphomyosot plus -lipoic acid
vs. -lipoic acid alone
Results of a prospective, reference-controlled
cohort study
Development of Diabetic
Polyneuropathy
Hyperglycemia
Oxidative stress Nonenzymatic
glycosylation
Destruction of
Reduction equivalents
decrease nerve sheaths Development of AGE
Free radicals Inflammatory Thickening of Radial/anchor fibres
increase cytokines increase basem. memb. thickened/rigid
NFkB increases in edema in Circ. dist. peri-/ Disturbed
defensive cells nerve sheaths endoneurium lymph function
Inflammatory Colloidal osmotic
cytokines increase
Matrix edema pressure increases
Lyphosot® (Drops)
D12
D6
D5
D4
D3
Geranium
Apis Juglans Urtica Myosotis Pinus Scrophularia Fumaria
robertianum
regia Urens arvensis sylvestris nodosa officinalis
Fucus Sarsaparilla Natrum Gentiana Veronica Equisetum Calcium Teucrium
Vesiculosis sulphuricum lutea officinalis hyemale phosph. scrorodonia
Single Homeopathic Remedies
Response Variables
Patient
Efficacy Tolerability
compliance
Extent of neuropathic disturbances: ADR Compliance
- pain (needle) Global with treatment
- touch (monofilament) assessment
- feeling of numbness
- tingling (paraesthesia)
- spontaneous pain (nocturnal)
- reduction in pain on movement
Edema in foot/lower leg
Time at which symptoms improved
Treatment result
Time of First Improvement
Alpha-lipoic acid (n = 114)
Lymphomyosot + alpha-lipoic acid (n = 155)
No. of patients (in %)
50
40
30
20
10
0
th
s
s
s
t
en
th
th
th
on
on
on
on
em
m
m
m
m
ov
1
-2
-3
-6
<
pr
r1
r2
r3
im
te
te
te
No
Af
Af
Af
Treatment Results
Alpha-lipoic acid (n = 114)
Lymphomyosot + alpha-lipoic acid (n = 155)
No. of patients (in %)
60
50
40
30
20
10
0
Very good Good Moderate Not
successful
Global Asessments
Lymphomyosot +
-Lipoic acid
Response variable -lipoic acid Statistics
(n = 114)
(n = 155)
Onset of effect ++ +++ Ptotal = 0.0058
Treatment result ++ +++ Ptotal = 0.0018
Tolerability ++ +++ Ptotal = 0.0332
Compliance with +++ +++ Ptotal = 0.2166
treatment
Osteopenia
Osteopenia
Osteoporosis
Osteomalacia
Primary hyperparathyroidism
Malignant disease
WHO’s Definition of Osteoporosis
Metabolic bone disease in which there is both a
decrease of normally mineralized bone and the
disturbance in bone micro-architecture
Risk of fractures even in the absence of trauma
Diagnosis of Osteoporosis
X-Ray no good
Scans
DEXA (dual energy X-Ray absorptiometry)
CT scans
Ultra sound at the heel
Normally uses a T-score
T score = BMD-YN
SD
BMD= Bone mineral density, YN =Young normal, SD= standard deviation
WHO’s Criteria for Osteoporosis
Normal BMD> -1.0 below the
young adult range
Low bone mass BMD - 1 to -2.5 below
Osteoporosis BMD < -2.5 below
Severe osteoporosis BMD < -2.5 range and
the patient has one or
more fractures
Risk Factors for Osteoporosis
Female, especially postmenopausal
Race/Ethnicity Rare in African Americans and Mexican
Americans common in Caucasians and Asians
Diet: high protein diet increases risk
Smoking
Alcohol
Inactivity
Leanness
Coffee ingestion
Diseases associated with secondary osteoporosis
Cushing’s syndrome, Thyroid hormone suppressive
therapy, previous gastric surgery
Osteoclasts/Osteoblasts
INTERLEUKIN 1 TGFβ
TNF Stimulates
Stimulate the osteoblasts
osteoclasts
TH3 cells
TISSUE INFLAMMATION TISSUE REPAIR
AND DEGRADATION (free radicals)
Osteoporosis Bone mineralization
Treatment of Osteoporosis
Diet low in protein
Weight bearing activity
Stop smoking
Low alcohol intake
No coffee
Adjuvant
Isoflavones (Equifem-Balance 2-4 capsules per day)
Calcium 1000-1500 mg/day
Vit D 400 IU per day
Free amino acids
Osteoporosis
SYMPTOMATIC OSTEEL
BASIC REMEDY CALCOHEEL
HOMACCORD
RANUNCULUS-HOMACCORD
COLOCYNTHIS-HOMACCORD
+
DETOX-KIT
DETOXIFICATION
SUPPORT
GALIUM-HEEL
REGULATION IMMUNOMODULATION
Traumeel
+ CELLULAR ACTIVATION
UBICOENZYME
INDUCE
VICARIATION FUNICULUS UMBICALIS SUIS-
TISSUE AND
PHASE
INJEEL
REMEDY Tissue remedy of choice
SUMMARY
THANK YOU
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