NUTRITION

7- Diet & Nutrition in Oral Health

1. Four interrelated factors of the oral infectious process: a. Susceptible host or tooth surfaceb. Microorganisms present (Streptococcus mutans, Lactobacillus casein, Streptococcus sanguis)c. Fermentable carbohydrates (substrate for bacterial metabolism)d. Time or duration in the mouth for the bacteria to metabolize carbohydrate

2. Development of caries is a pathologic process of demineralizationa. Plaque bacteria feed on fermentable carbohydrates; Form acid, causes a drop in pH (<5.5)

environment for demineralization; Bacteria destroy the dentin while acid destroy mineralized tissue3. Factors affecting food cariogenicity:

a. Frequency of consumption of fermentable carbohydratesi. Any monosaccharides or disaccharides (simple sugars), including: glucose, fructose, maltose,

lactose, and sucrose; Starches can contribute to caries if they are held in the mouth long b. Length of exposure of teeth to food and beverages

i. Fermentable carbohydrate consumed decline in pH is initiated within 5-15 minutes and lasts about 20-30 minutes

c. Food form (adherence, exposure time)d. Sequence of eating foods and combination of foods (buffering effects of certain foods)e. Nutrient composition of food affects its ability to create an acidic environment

i. Dairy products have calcium and phosphorus that act as buffering and remineralizing agentsii. Protein foods & fats (butter/oil) are not cariogenic- no fermentable substrate

iii. Relative cariogenicity of a food is not correlated with its carbohydrate (sugar) contentf. Noncarbohydrate sweeteners influence caries in ways

i. Xylitol- anticariogenic- prevents plaque from recognizing an acidogenic food; Other non-caloric sweeteners such as saccharin, cyclamate, and aspartame are non-cariogenic

4. Periodontal disease and gingivitis result from plaque oral bacteria causing infectionsa. The plaque from the gingival sulcus produces toxins that destroy tissue and permit loosening of teeth b. Factors important for resistance of the gingiva to bacterial invasion are:

i. Oral hygieneii. Integrity of the immune system to resist infection

iii. Nutrition: deficiencies in vitamin C, folate and zinc increase the permeability of the gingival barrier at the gingival sulcus increasing risk of development of periodontal disease

5. Caries and periodontal disease can be prevented and/or arrested with plaque control, dietary modification, and the use of fluoride

a. Tooth brushing/ mechanical cleaning procedures are the most reliable means of controlling plaqueb. Dietary advice should be based on food records or recalls

i. Diet pattern counts most : Increased freq. of cariogenic food consumption = increased caries risk; Oral contact time is key; Considered safe: 3 meals, no more than 3 snacks

c. General micronutrient adequacy of the diet (risk for vitamin C, folate & zinc)d. Fluoride sources should be identified and if needed, providede. Patients with salivary glands that are not functioning properly may benefit from an artificial saliva spray

containing calcium, phosphate and fluoride ions; Chewing gum also stimulates salivary flow6. Fluoride : Mechanisms of Action

a. Tooth Enamel : Reduces Enamel Acid Solubility (Demineralization); Enhances Remineralization; Alters Enamel Structure: Hydroxyapatite Fluorapatite (less acid soluble)

b. Bacteria : Inhibits Bacterial Growth (Bacteriostatic); Kills Cariogenic Bacteria (Bactericidal)c. Optimum fluoride concentration in drinking water is between 0.7 to 1.2 ppm

i. Levels > 2.0 ppm increase risk for Dental Fluorosis: enamel hypomineralization; maximum sensitivity to fluorosis between 11 months to 7 years (when permanent teeth are developing

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8- Iron

1. Iron Distribution in the Bodya. Hemoglobin (oxygen transport) 69% Ferritin (intracellular storage) 27%

2. Most of the daily iron required is recycled via the reticuloendothelial system3. Two Dietary Types of Iron

a. Heme iron - Flesh sources (Meat, fish, poultry)b. Non-heme iron - Plant sources; vitamins & supplements

i. Transport by the divalent cation transporter (DCT1 or DMT1)ii. Requires solubilization from oxidized 3+ ferric to the reduced ferrous 2+

1. Ferric reductase (ferric/cupric duodenal cytochrome b reductase, Dcytb) at the brush border reduces Fe+3 to Fe+2

2. If ingested non-heme iron is not reduced, the alkaline environment of the small intestine will favor formation of ferric hydroxide and this may prevent absorption

4. Dietary components influence bioavailability of non-heme iron a. Enhance non-heme absorption by improving solubility, reducing ferric iron

or chelating iron to organic (absorbable) compounds that are absorbedi. Factors Enhancing Iron Absorption: Sugars; Acids; Meat, Ethanol

b. Reduce absorption of non-heme iron by influencing solubility or pHi. Inhibitors of Iron Absorption

1. Polyphenols (e.g. Tannic acid in tea and red wine); Oxalate (Grains, fruit, vegetables); Phytates (Legumes, grains, rice, vegetables); Minerals (Calcium; Zinc; Manganese; Nickel)

c. Efficiency of absorptioni. Transporter mediated pathways- Saturable & regulated by hormones (Hepcidin for Fe)

ii. Parcellular- Not regulated and non-saturable5. Iron once in the Enterocyte…

a. Stored complexed to ferritin or used within cellb. Exported across the basolateral membrane by ferroportin

i. Iron must be oxidized to 3+ by hephaestin or ceruloplasmin before it can be bound by transferrin (Copper is required as a cofactor)

ii. Transferrin carries iron in circulation where it can be transported at the basolateral membrane via transferrin receptors facilitated by HFE

6. Stores of iron within the enterocyte regulate iron transport a. If iron stores are low, absorption can be up-regulated by increased enzyme

activity at the luminal membrane along with decreased hepcidin production by the liver more iron transported across intestinal cells into the body

b. When hepcidin increases, stores of iron in the enterocyte increase due to decrease in both basolateral transport & luminal uptake of non-heme iron

7. Excretion- There is no physiologic mechanism to excrete excess iron. Excretion occurs mostly through losses such as shed mucosal and skin cells and in secretions and in menstrual losses

8. Excess Intake of Iron a. Hepcidin and Iron Overload (Hemochromatosis)

i. Defective hepcidin due to hepcidin gene defectii. Defective regulation of hepcidin expression by liver by HFE gene defect

iii. Defective ferroportinb. Pathogenesis of Iron Overload

i. Free iron circulates; ROS species generated by free iron; Insoluble iron complexes deposited in organs; End organ accumulation of ironTissue damage

c. Bantu iron overload- Genetic predisposition to excess absorption; More diet responsive

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9. Iron Deficiency a. Most common nutrient

deficiency world-wideb. Populations at risk:

Infants/young children, Adolescents, Menstruating females, Pregnant women, Malabsorption syndromes, Intestinal parasites, Vegetarians, Athletes, Chronic gastrointestinal or other losses

c. Symptoms may occur prior to anemia

i. Results in: Anemia, Fatigue and lethargy, Cold intolerance, Impaired psychomotor development, intellectual performance and/or immunity, Adverse pregnancy outcomes, Increased risk lead poisoning

d. Treatment of Iron Deficiencyi. Assess etiology and address abnormal losses; Iron supplements effective;

Can take with low dose vitamin C; Parenteral iron if necessary

9- Water Soluble Vitamins: Vitamin C, Thiamine and Niacin

1. Vitamin C = Ascorbic Acid (active form L-ascorbic acid)a. Functions as an electron donor (antioxidant)- During oxidation of vitamin C, a

free radical form is produced that is more stable than many other free radicals b. Ascorbic Acid

i. Synthesized by plants from glucose and fructoseii. Destroyed by : Oxidation; Heat; Exposure to air or alkaline medium;

Contact with copper and iron oxidizes it to dehydroascorbic acid (DHAA)iii. Food Sources- Widely distributed in anything that is fresh and rapidly growing

c. Roles include:i. Collagen synthesis

ii. Carnitine synthesis iii. Neurotransmitter metabolism iv. Antioxidant function v. Regeneration of reduced vitamin E

d. Excreted by kidney as: Ascorbic acid; Can be metabolized to oxalic acid which may potentiate oxalate nephrolithiasis

e. Supplemental use for decubitus ulcers may enhance wound healingf. Vitamin C Requirements:

i. Vitamin C Deficiency: Scurvy : prevented by 10 mg/day1. Weakness and lassitude2. Skin and soft tissue (Petechial hemorrhage; Perifollicular

hyperkeratosis; Ecchymosis; Impaired wound healing)3. Impaired bone growth and bowing; Subperiosteal hemorrhage; 4. Swollen gums that easily bleed; Tooth loss5. Depression; Confusion, hysteria; Hypochondriasis

g. Vitamin C Excess: UL = 2 g/day (based on diarrhea and bloating)

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2. Thiamine (Vitamin B1) a. Pyrimidine and thiazole groups with methylene bridge; 0 (free form- usually found in plants) to 3 phosphates

b. Sources: Whole & Enriched grains/cereals; Some vegetables and legumes; Meats, Dairyc. Thiaminases (Fish, shellfish, ferns, microorganisms): Degrade thiamine d. Antithiamine compounds (Ferns, teas, betel nuts): Forms oxidized inactive compoundse. No UL = no toxicity; Body pool=30 days of RDA (50% in muscle); Rapid turnover

f. Co-factor for a limited number of enzymesi. NADPH biosynthesis- Transketolase in pentose phosphate pathway

ii. Energy metabolism- Dehydrogenases: e.g. Pyruvate dehydrogenase

iii. Nerve function - Synthesis of acetylcholine, glutamate and GABAg. Thiamine Deficiency

i. Erythrocyte transketolase activity most accurate functional assay ii. Metabolic Effects: Cellular energy failure; Accumulation of lactate; Reduction in TCA

intermediates; Reduction in high energy phosphate & neurotransmitter synthesisiii. Beriberi has two overlapping forms

1. Dry - Distal peripheral neuropathy; Diminished reflexes; Calf tenderness2. Wet - Tachycardia and low peripheral resistance; Edema;

Cardiomegaly and CHF; Peripheral neuropathyiv. Wernicke-Korsakoff Syndrome suspected that a genetic predisposition may exist

1. Early: W. encephalopathy- Opthalmoplegia; Ataxia; Confusion2. Later:K. psychosis- Amnesia; Confabulation; Loss of spontaneity/ initiative

h. Risk Factors for Thiamine Deficiencyi. Poor intake OR intake of foods with thiaminases or antithiamines ii. Alcoholism ↓ GI transport out of enterocyte ↓ Phosphorylation to diphosphate ↓ liver stores with cirrhosis

iii. Maternal thiamine deficiencyiv. Bariatric surgery; Persistent vomiting (Hyperemesis gravidarum); Refeeding syndrome

3. Niacin (Vitamin B3) a. Sources: Whole grains (bioavailability in grains requires alkali to release

niacin), Meat and fish, Yeast, nuts, Eggs, Milk, Tryptophan (Precursor)b. Biochemical Roles of Niacin

i. Energy utilization - Oxidation of glucose and fatty acidsii. Synthesis of - Fatty acids, cholesterol; Steroid hormones and glutamate

iii. Modification of proteins - DNA repair; Cell differentiation and replicationiv. High dose: ↓ triglycerides and ↑ HDL-C

c. Niacin Toxicity i. Vasodilatory flushing (partly due to histamine)

ii. GI intolerance; Hepatotoxicity; Hyperuricemia and gout (Niacin competes with uric acid for excretion); Glucose intolerance and Decreased insulin sensitivity

d. Risk for Niacin Deficiencyi. Diets characterized by the 3 Ms: Maize: untreated with base; Meat: poor

quality and high fat content; Molasses: high CHO diet low in niacin & tryptophanii. Hartnup’s disease; Carcinoid tumors

e. Niacin Deficiency : 4 Ds of Pellagrai. D ermatitis in sun-exposed areas of the skin (Casal’s necklace)

ii. D iarrhea due to mucosal atrophy and inflammationiii. D ementia- Anxiety, depression and insomnia; Delirium and

hallucinations; Neuropathy and muscle weaknessiv. D eath

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10- Water Soluble Vitamins: Folate and Vitamin B12

1. Folate and vitamin B 12: critical co-enzymes; By inhibiting the MS reaction, B12 deficiency causes a functional folate deficiency: the methylfolate trap; Patients with B12 deficiency present with elevated levels of folate

2. Folic acid (B9)a. Folate metabolism supports two critical, and competing

pathways: biological methylation and nucleotide synthesisi. Is the essential co-factor for the rate-limiting reaction in

DNA synthesisb. Deficiency risk: Generalized poor diet; Ethanol abuse (Ethanol interferes with folate absorption and

metabolism); Malabsorptive disorders; Drugs interfering with folate absorption/ metabolismc. Folate status can be assessed by the

concentration in plasma and in RBCsi. Plasma folate reflects recent intake, decreases 1st

ii. RBC folate remains relatively stable; decreased RBC folate occurs in more chronic deficiency

d. Folate Deficiency : manifestations reflect the vitamin’s critical functions in rapidly proliferating cells; results in decreased regeneration of tissues with rapid turnover

i. Megaloblastic (macrocytic) anemiaii. Megaloblastosis of GI epithelium:

diarrhea and malabsorptioniii. Myelomeningocoele (spina bifida)

e. Folate metabolism: the foundationstone of modern antibiotics and cancer chemotherapy

i. Methotrexate functions as an inhibitor of dihydrofolate reductase (inhibits DHF THF)

3. Vitamin B12 a. Cofactor for conversion of:

i. Homocysteine to methionine ii. Methylmalonyl CoA to succinyl CoA

1. Abnormal accumulation of methylmalonic acid is indicator of B12 deficiencyb. Sources: animal foods (plants do not synthesize B12)c. Absorption- Vitamin B12 in food is bound to protein

i. Low acid states (aging and due to acid-reducing medications) may impair this stepii. Intrinsic factor (produced in stomach) binds B12 in the intestine and facilitates absorption

d. Vitamin B12 deficiency :i. Megaloblastic anemia : due to trapping of folate in irreversible rxn to methyl THF

ii. Neuronal death in spinal cord (combined subacute degeneration ) iii. Encephalopathy, myelopathy, peripheral neuropathy, and optic neuropathyiv. Diarrhea and malabsorption

e. Risk for vitamin B12 deficiency:i. Vegans and Infants of vegan mothers who rely only on breastfeedingii. Conditions resulting in diminished secretion of gastric acid and/or intrinsic

factor: Use of drugs that reduce gastric acid secretion; Atrophic gastritis – Reduced gastric acid; Pernicious anemia– loss of intrinsic factor secretion and gastric acid

4. In persons 51 years and older it is recommended that most of the RDA for vitamin B12 be consumed in the crystalline form, reflecting the increasing prevalence of atrophic gastritis and difficulty with B12 digestion

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11- Fat Soluble Vitamins

1. General propertiesa. Contains only carbon, hydrogen & oxygen; May have precursors or pro-vitaminsb. Absorbed into lymphatic systemc. Daily intake is not critical; Intake in excess of daily needs are storedd. Deficiency symptoms slow to develop; May be toxic at relatively low concentrations

2. Vitamin A (retinoids)a. Includes

i. Preformed vitamin Aii. Provitamin A carotenoids produced by plants & algae

b. Sources:i. Vitamin A Animal sources- eggs, meat, dairy

ii. Beta-carotene sources- Green, leafy vegetables; intensely colored fruits and vegetablesiii. Raw foods have the lowest bioavailability; cooking helps liberate

c. Digestion and Absorption i. Retinol absorption is carrier mediated

ii. Carotenoids absorbed passively with digestion of fat iii. Carotenoids cleaved to retinol in the enterocyte; adequate vitamin A

stores inhibit cleavageiv. Vitamin A is transported to the liver where it can be stored as retinyl

esters or transported from the liver to other tissuesv. Retinol binding protein facilitates transport in the circulation

d. Biological Roles of Vitamin A i. Vision

1. Dark adaptation2. Epithelial tissue

ii. Bone growthiii. Reproductioniv. Cell divisionv. Cell differentiation

vi. Regulation of the immune systeme. Biological Roles of Carotenoids

i. Provitamin A: α-carotene; ß-carotene; ß-cryptoxanthin

ii. Antioxidant that protects cells from free radicals; associated outcomes such as “prevention” of macular degeneration

f. Assessment of Vitamin Ai. Risk for deficiency

1. Poor diet2. Malabsorption3. Liver disease

ii. Risk for excess 1. Supplements and polar bear liver2. Renal disease3. Carotenoids do not lead to vitamin A toxicity

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3. Vitamin D a. Forms

i. Vitamin D 2 - Ergocalciferol1. Sources: Plants, fungi, invertebrates; Supplements and fortified foods

ii. Vitamin D 3 - Cholecalciferol1. Sources: Skin synthesis; Animal foods; Supplements and fortified foods

b. Advantages to D3; D3 is more effective ati. Increasing 25-OH vitamin D concentration

1. Obesity is inversely associated with circulating 25-OH vitamin D concentration

ii. Suppressing PTH1. Elevated PTH may indicate deficiency of vitamin D

c. Roles of Vitamin Di. Calcium- Absorption & Homeostasis

ii. Bone healthiii. Muscle function

d. Vitamin D might Influence DM Riski. Mediated by calcium

ii. Modulation of autoimmunityiii. Increased beta cell insulin secretioniv. Increased insulin sensitivity v. Reduced inflammatory cytokines

e. Vitamin D Deficiency i. Bone

1. Children: Rickets2. Adults: Osteomalacia; Osteopenia

ii. Myopathy and weaknessiii. Risk factors

1. Infants who are exclusively breastfed2. Limited sun exposure3. Greater skin melanin content4. Age5. Renal disease6. Liver disease7. Drugs8. Fat malabsorption syndromes (Cystic Fibrosis; Crohn’s

disease; Celiac disease; Surgical resection of small intestine)f. Vitamin D Excess

i. Usually from supplements or Rx; Not from UV exposureii. Symptoms due to hypercalcemia

1. Nausea and vomiting2. Elevated serum calcium concentrations

a. Mental status changes; Arrhythmia; Nephrolithiasis; Calcinosis

g. Assessment of Vitamin D Statusi. Vitamin D status reflected by

1. 25-OH (stable, active form) vitamin D concentration

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4. Vitamin E a. Limited food sourcesb. Biological Roles

i. Antioxidant (Reduced by vitamin C)ii. Immune function

iii. DNA repairc. Is absorbed with micelles and transported to liverd. Vitamin E Deficiency

i. Deficiency associated with1. Neuropathy2. Myopathy3. Retinopathy4. RBC hemolysis (RDA is based on the amount needed to

prevent oxidative damage)ii. Risk factors

1. Premature very low birth weight infants 2. Fat malabsorption3. Rare genetic disorders (eg. α-tocopherol transfer protein

defects)e. Vitamin E Excess due to supplement use

i. Bleedingii. May interfere with vitamin K metabolism

iii. Supplemental doses above 400 IU not routinely recommended

5. Vitamin K a. Sources: Green leafy vegetables & oilsb. Biological Roles

i. Cofactor for the γ-carboxylation of Glu to Gla in proteins involved in

1. Coagulation; Bone mineralization; Regulation of calcification

c. Vitamin K Deficiency i. Results in coagulopathy & bleeding

ii. Risk factors1. Malabsorption2. Liver disease3. Poor intake4. Alcoholism

iii. Babies are born deficient - Must be supplemented at birth to prevent hemorrhagic disease of the newborn

iv. Warfarin inhibits the vitamin K cycle by acting on the enzymes required for regeneration of active vitamin A, thus reduces coagulation and prolongs time to clotting

v. Warfarin use in pregnancy results in embryopathy

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12- Nutrition in Acute Illness

1. Nutrition Goals in Hospitalized Patients= Maintenance of Lean body mass and/or body weight and Physiologic function

2. The Stress Response - The Metabolic Response to Illnessa. Response proportional to severity of illnessb. Hypermetabolism : increased energy needs proportional to severity of illness

and fever which activates sympathetic nervous system and catecholamines, inflammatory cytokines, accelerated catabolism and futile cycles

c. Altered protein synthesis and catabolism i. Accelerated protein catabolism of muscle, albumin and other proteins.

ii. Altered protein synthesis in liver favoring synthesis and secretion of acute phase proteins and reduction in synthesis negative acute phase proteins (albumin)

1. Albumin is not an indicator of protein nutrition in acute illness settingiii. Results in protein catabolism, which is measured by urinary nitrogen excretion

d. Hyperglycemia due to inability to suppress gluconeogenesis ( glucagon) even when blood glucose is normal or elevated and insulin resistance

e. Edema due to hypoalbuminemia, increased capillary “leakiness”, and water retentionf. Response can occur in well-nourished pt rapidly after severe injury or surgery

i. The dysregulation of protein metabolism along with other elements of the stress response creates a picture of kwashiorkor even when protein nutrition hours or days previous was adequate

g. Mostly due to resting expenditure (Range 1.3 to > 2 times normal)3. Adverse Effects of PEM: Mortality; Prolonged hospitalization; Infection; Impaired wound

healing/ skin integrity; Impaired balance and increased weakness4. Identifying Protein Energy Malnutrition in Hospitalized Patients

a. Weight and weight change (Influenced by hydration, Scale used)i. BMI < 18.5 kg/m2

ii. Involuntary loss of > 10% usual weight over 3-6 monthsb. Physical Exam (Muscle wasting; Loss of subcutaneous fat)c. Recent intake; Functional status

5. Who Benefits from Nutrition Support ?a. Pre-operative patients with moderate-to-severe PEMb. Inpatients with severe alcoholic liver diseasec. Patients undergoing bone marrow transplantationd. Acutely ill patients with moderate-to-severe malnutrition who will be unable

to meet at least 80% of their needs ad libitum in the next 48 hre. An acutely ill patient who is mildly malnourished or well-nourished but is

unlikely to meet >80% of their nutritional needs within the next 7-10 days6. Nutrition support

a. Enteral nutrition (via the gut)i. Tubes placed (nose, mouth, stomach, abdominal wall)

ii. Possible benefits of enteral feeding1. Minimizes complications of parenteral nutrition

iii. Complications of Enteral Feeding1. Tube placement; Aspiration pneumonia; Diarrhea

iv. Enteral nutrition formulas: Water; Macronutrients; Fiber; Micronutrients; Specialized formulas (e.g. omega 3 fatty acids)

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b. Parenteral nutrition (Bypasses the gut: intravenous feeding)i. Contains: Water; Macronutrients; Electrolytes (minerals); Vitamins and trace elements

ii. Total parenteral nutrition (TPN)1. High osmolality requires administration in vena cava; Meets energy & protein needs

iii. Peripheral parenteral nutrition (PPN)- Infused through smaller peripheral vein1. Lower osmolality due to risk of phlebitis; May not meet energy or protein needs

iv. Complications of Parenteral Nutrition1. Infection; Thrombosis; Hyperglycemia; Hypertriglyceridemia2. Refeeding syndrome- driven by carbohydrates; Overfeeding

7. Refeeding Syndrome a. Occurs in patients with PEM or poor intake when

carbohydrate is refed; Usually within hours to 3 days of refeeding

i. The insulin response and subsequent intracellular transport/ sequestration of glucose, electrolytes and thiamine can lead to serious consequences

b. At risk:i. Recent weight loss, especially if rapid;

Starvation/ Anorexia nervosa; Inadequate intake > 2 weeks; High output electrolyte losing disease states (E.g. diarrhea or frequent vomiting); Alcoholism

c. Prevention of Refeeding Syndromei. Replete all electrolytes prior to initiation of

nutrition support; Especially phosphate, potassium, magnesium

ii. Monitor and replete electrolytesiii. Thiamine repletion

8. Don’t overfeed- This may increase the risk of hyperglycemia, hypertriglyceridemia, and fat overload syndrome (a rare problem that is manifested when the reticuloendothelial system is overloaded with fat, usually due to IV administration)

9. Key Issues in Nutrition in the Elderly a. Atrophic gastritis leads to decrease in gastric acid

i. Vitamin B12 digestion and reduced intrinsic factorii. Reduced mineral absorption

b. Bone loss frailtyi. Reduced vertical height

ii. Reduced skin synthesis of vitamin Diii. Reduced liver or renal hydroxylationiv. Reduced intestinal calcium absorption

c. Dental health and tooth loss i. Sarcopenia

ii. Age related loss of muscle massiii. Possibly an inflammatory condition

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