Wednesday, 26 November 2014

HEALTH BENIFITS OF TRUE CINNAMON

Health benefits of True Cinnamon
What is True Cinnamon?
Sri Lankan ceylon is considered as ture cinnomon. True Cinnamon is a spice which is taken from the inner bark of some genus Cinnamomum trees. There is an alternative to true cinnamon and it is known as Cassia.



What is the difference bitween True Cinnamon and Cassia ?
Both true cinnamon and cassia are coming under same genus which is called Cinnamomum . Some species of genus Cinnamomum are known as true cinnamon and some are known as cassia.

Sciencetific Name of True Cinnamon
Cinnamomum zeylanicum /Cinnamomum verum

Sciencetific Name of Cassia
Cinnamomum cassia /Cinnamomum aromaticaum
Cinnamomum burmannii

Both above types share their characterstics such as blood sugar regulationsso on. When considering flavor profile of cassia and true cinnamon, cassia cinnamon has stronger and hotter taste than true cinnamon and also color of it is darker than true cinnamon.

The major problem regarding these two types is cumarin content. Cumarin content is not equal of both two types. Cassia cinnamon contains comparatively higher amont of cumarin than Ceylon cinnamon. Cumarins are naturally occuring fragrant organic compound in the benzopyrone chemical class that can be toxic in larger amounts. These toxicities tend to effect the liver and nervous system most directly. The level of naturally occurring coumarins in Ceylon cinnamon is ver low and that amount could not cause health risk. But The level of naturally occurring coumarins in Cassia cinnamon is compartively higher. The amount of cumarin content in ceylon cinnamon is onlty
0.0004% against 5% found in cassia cinnamon.


If Cassia cinnamon consume substantial amounts on regular basis, it may pose a risk to some individuals. There fore consumption of cassia cinnamon in larger amounts should be avoided.








How to identify True Cinnaon and Cassia Cinnamon?
If your cinnamon shows multiple layer of thinner bark, it is Ceylon/true cinnamon and your cinnamon shows thick single layer bark, it ia Cassia cinnamon.

So, please pay your attention to identify true cinnamon, before you consume cinnamon for the betterment of your health.





Health Benifits of Cinnamon

Blood Sugar Control
If someone use half tea spoon of powdered cinnamon, there are evidance that it will significantly reduce blood sugar levels, LDL(bad) cholesterol, triglycerides and total cholesterol levels in patient with type 2 diabetes.

There are many cinnamon supplimenataions available tody if you are spending sedentary life style or if you have poor dietary choices to treat your diabetes.

Cinnamon can increase glucose metabolism of the body by 20-fold and it significantly improves blood sugar regulation. Cinamon contains many bio active compounds and they act as an insulin substitute.

Cinnamon contains higher amount of fiber and it may slow the empting of stomach after the meal to reduce sharp rices in blood sugar and improve the effectiveness or sensitivity of insulin. Polyphenols from cinnamon act as insulin sensitizer and antioxidents. As well as a bioflavonoid in cinnamon called proanthocyanidin may alter insulin-signaling activity in fat cells. All above factors effcts to control blood sugar level directly or indirectly.

Lowering LDL cholesterol and triglycerides
If there are evidances available to say cinnamon reduce LDL cholesterol and triglyceride by inderectly. It is found that cinnamon reduce triglyceride(23%-30%), LDL cholesterol(7%-27% ) and total cholestarol(12% - 26%). Statistically significant decrese can be observed in total cholestarol level, LDL, triglyceride and increase good cholestarol(HDL).



Protect against Heart Disease
Cinnamon conatin comparatively more fiber. As we as this contain much calcium. Due to cinnamon contain both fiber and calcium, it is grat for heart heath. By breaking down cholesterol, body can produce bile salt. Together with fiber and calcium help transport bile salts outside the body. Due to that break down of cholesterol will be enhanced. This directly translates to lower cholesterol levels which protect the heart from blockage and arteries from atherosclerosis.



Protect fron Cancer
According to study done by United States Agriculture Department, they have found that cinnamon extract directly effects on leukaemia and lymphomas. The cinnamon extract block the path of certain component that were important for regeneration of the cells. Further it is inhibited multification of cancerous cells and slowly reduced their spread. It was examined that the amont of extract will be high, results also will be better. And also extarct inhibit the growth of unhealthy cells only.


Relieves Arthritic  and Muscle Pain
Cinamon contain a very strong anti-inflammatory and antibacterial compound known as cinnamomum. It is a great home remedy for arthritic pain. It has natural heating mechanism provides added relief to aching joints.






Helps in digestion
Cinnamon is packed with mineral manganese, fibre, essential oils and calcium. The calcium and fibre combine with bile salts and help in their transport outside the body. The essential oils, help regulate the action of gastric juices on food, improves digestion, assimilation and its anti inflammatory properties helps reduce the inflammation caused due to indigestion, Irritable Bowel Syndrome and ulcers. Moreover the fibre content helps to relieve constipation and diarrhoea.




Helps with weight loss
Cinnamon has great digestive properties, it helps with weight loss by regulating the breakdown of carbohydrates and the production and use of insulin by the body. It also helps improve the digestion and assimilation of food within the body, helping one lose weight.



Helps beat acne
Cinnamon is a common spice and flavoring agent but the essential oil it contains also has strong anti-microbial properties. The water activity of honey is very low and this means that it does not contain a lot of moisture which can promote the growth of microorganisms. Considering that pimples often arise from an infection within the pores of the skin, combining cinnamon with honey is an effective remedy.



Helps cure a cold and cough
Cinnamon is known for its antibiotic and body warming properties, cinnamon is a formidable remedy against a cold and cough. It not only helps to relieve the congestion commonly experienced with a cold, it is also great for a sore throat when combined with ginger, tulsi and honey



















Monday, 24 November 2014

HEALTH BENIFITS OF COCONUT OIL

Health Benefits of Coconut Oil


Coconut oil the best oil in the earth and so it is categorized as a 'super food”. It has unique combination of fatty acids and these fatty acids have profound positive effects on health. This includes fat loss, reducing risk of heart diseases, better brain function and various other helpful benefits.

Brief composition of Coconut oil


More than ninety percent of coconut oil consists of saturated fats, along with traces of few unsaturated fatty acids, such as monounsaturated fatty acids and polyunsaturated fatty acids. Virgin coconut oil is no different from this.
  • Saturated fatty acids: Most of them are medium chain triglycerides, which are supposed to assimilate well in the body’s systems. Lauric acid is the chief contributor, representing more than forty percent of the total, followed by capric acid, caprylic acid, myristic acid and palmitic.
  • Polyunsaturated fatty acids: Linoleic acid.
  • Monounsaturated fatty acids: Oleic acid.
  • Poly-phenols: Coconut contains Gallic acid, which is also known as phenolic acid. These polyphenols are responsible for the fragrance and the taste of coconut oil and Virgin Coconut Oil is rich in these polyphenols.
  • Certain derivatives of fatty acid like betaines, ethanolamide, ethoxylates, fatty esters, fatty polysorbates, monoglycerides and polyol esters.
  • Fatty chlorides, fatty alcohol sulphate and fatty alcohol ether sulphate, all of which are derivatives of fatty alcohols.
  • Vitamin E, vitamin K and minerals such as iron.


Unique Combination of Fatty Acids and its Powerful Medicinal Properties

When we are consuming various types of foods, it contains various type of fatty acids. Specillay long-chain fatty acids and medium-chain fatty acids. They may be saturated or unsaturated. Unsaturated fatty acids are harmfull than saturated fatty acids. Coconut oil contain higher percentage of medium-chain fatty acids which is more help benificial. Specility of medium-chain fatty acids in coconut oil are metabolized differently.
They go straight to the liver from the digestive tract, where they are used as a quick source energy or turned into so-called ketone bodies, which can have therapeutic effects on brain disorders like epilepsy and Alzheimer’s.
Note - Medium chain triglycerides in coconut oil , which are metabolized differently and can have therapeutic effects on several brain disorders.

 Increasing Energy Expenditure by Helping Burn More Fat

The biggest health problems in the world is obesity. Many people think reason for the obesity is fatty foods, high calory foods or junk foods. But that is only one reason.Different foods affect to the body and hormones in different ways. So many other factores effects to obesity in addition to fatty or high calorie foods.
The medium-chain triglycerides (MCTs) in coconut oil can increase energy expenditure compared to the same amount of calories from longer chain fats.
According to a sciencetific study, it is found that 15-30 grams of MCTs per day increased 24 hour energy expenditure by 5%,totalling about 120 calories per day.


Reducing Hunger by Making Eat Less

One interesting feature of coconut oil is that it can reduce your hunger. This may be related to the way the fatty acids in it are metabolized, because ketone bodies can have an appetite reducing effect .
If this effect were to persist over the long term, it could have a dramatic influence on body weight over a period of several years.
Note : The fatty acids in coconut oil can significantly reduce appetite, which may positively affect body weight over the long term.

Acting as an energy source
MCTs in coconut oil get shipped to the liver and turned into ketone bodies, they are often used in epileptic patients to induce ketosis while allowing for a bit more carbs in the diet .
These ketone bodies can act as energy sources for cells when lacking of sugar for energy generation. There ketone bodies specilally utilized by brain cells and nurones.
Note : The MCTs in coconut oil can increase blood concentration of ketone bodies, which can help to use as an energy source.


Effects on Heart diseases

There is a misconception spread among many people that coconut oil is not good for heart health. This is because it contains a large quantity of saturated fats.In reality, coconut oil is beneficial for the heart. It contains about 50% lauric acid, which helps in actively preventing various heart problems like high cholesterol levels and high blood pressure. The saturated fats present in coconut oil are not harmful as you commonly find in vegetable oils. Coconut oil does not lead to increase in LDL levels, and it reduces the incidence of injury and damage to arteries and therefore helps in preventing atherosclerosis.

Effects on Digestion

Internal functions of coconut oil occur primarily due to it being used as cooking oil. Coconut oil helps to improve the digestive system and thus prevents various stomach and digestion-related problems including Irritable Bowel Syndrome. The saturated fats present in coconut oil have antimicrobial properties and help in dealing with various bacteria, fungi, and parasites that can cause indigestion. Coconut oil also helps in the absorption of other nutrients such as vitamins, amino acids and minerals


Effects on Immunity

Coconut oil is also good for the immune system. It strengthens the immune system because it contains antimicrobial lipids, lauric acid, capric acid and caprylic acid which have antifungal, antibacterial and antiviral properties. The human body converts lauric acid into monolaurin which research has supported as an effective way to deal with viruses and bacteria that cause diseases like herpes, influenza, cytomegalovirus, and even HIV. Coconut oil helps in fighting harmful bacteria like listeria monocytogenes and helicobacter pylori, and harmful protozoa such as giardia lamblia.

Effects on Skin care
Coconut oil is an excellent massage oil for the skin as well. It acts as an effective moisturizer on all types of skin, including dry skin. The benefit of coconut oil on the skin is comparable to that of mineral oil. Fortunately, unlike mineral oil, there is no chance of having any adverse side effects on the skin from the application of coconut oil. Coconut oil therefore is a safe solution for preventing dryness and flaking of skin. It also delays the appearance of wrinkles and sagging of skin which normally accompany aging. Coconut oil also helps in treating various skin problems including psoriasis, dermatitis,eczema and other skin infections. For that exact reason, coconut oil forms the base ingredient of various body care products like soaps, lotions, and creams that are used for skin care. Coconut oil also helps in preventing premature aging and degenerative diseases due to its well-known antioxidant properties.


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FACTORS EFFECTS ON OSTEOPOROSIS

Factors effects on osteoporosis

Among nutritional factors that cause bone loss, deficiencies in calcium, vitamin D, and more recently, protein have been shown to be associated with deficient skeletal growth or accelerated bone loss. Vitamin K deficiency may also be associated with risk of hip fracture. Dietary intake of phosphates may be increasing in some populations as a result of their use as food additives and the increase in intake of carbonated drinks. These drinks may have a deleterious effect on bone, because they have replaced milk in the diet of some young people, and because high intakes of phosphates stimulate the secretion of PTH, but there is no evidence so far that high phosphate intakes accelerate bone loss in humans.

Calcium intake, vitamin D and osteoporosis

In the elderly, several factors contribute to negative calcium balance. With ageing, calcium intake decreases because of reduced consumption of dairy products, and the absorptive capacity of the intestinal epithelium to adapt to low calcium intake is impaired. Exposure to sunlight and the capacity of the skin to produce vitamin D are also reduced. The capacity of the renal tubule to reabsorb calcium, and its responsiveness to PTH are impaired. Finally, the decease in glomerular filtration rate observed in the elderly may contribute to chronic hyperparathyroidism, favouring a negative bone mineral balance and thus osteoporosis. Increasing calcium intake is certainly an important strategy which is relatively easier to implement than other possible preventive measures.


Protein intake and osteoporosis

The mechanism whereby a low protein intake has adverse effects on bone may be due to inadequate production of IGF- 1, which exerts anabolic effects on bone mass, not only during growth, but also during adulthood. Protein replenishment in patients with hip fracture can improve not only BMD, but also muscle mass and strength. These two variables are important determinants of the likelihood and consequences of falling and thus incidence of osteoporotic fractures.

This observation underlines the importance of weight-bearing in the maintenance of bone mass. At the tissue level, immobilization results in bone resorption being greater than bone formation. At the cellular level, immobilization increases bone reabsorption by osteoclasts associated with a decrease in osteoblastic formation. The molecular signal(s) perceiving the reduction in mechanical strain associated with immobility has not been identified.



Risk factors for osteoporotic fracture
Although many risk factors for osteoporotic fracture have been identified, risk factors for different fractures may differ. For example, an early menopause is a strong risk factor for vertebral fractures, but not for hip fracture in later life. Risk factors may be causally related or indirect. While the former are amenable to personal modification, environmental or therapeutic manipulation, even indirect factors may be useful in identifying individuals at high risk.

Trauma
Fractures occur when skeletal loads, whether from trauma or the activities of daily living in the case of some spine fractures, exceed the breaking strength of bone. Falls are the most common cause of traumatic osteoporotic fractures. The annual risk of falling increases from about 20% in women aged 35–49 years to nearly 50% in women aged 85 years and over, and is 33% in elderly men . Although environmental hazards play a role in many falls, up to half the falls among the elderly are associated with organic dysfunction, including diminished perceptions of the lower extremities and postural control, gait abnormalities, muscular weakness, decreased reflexes or poor vision. In addition, chronic illnesses such as neurological disorders, heart disease, stroke, urinary incontinence, depression and impaired cognitive function increase the risk of falling. The proportion of falls associated with these problems increases with age , and the risk of falling is correlated with the number of comorbid conditions present.


Low bone density
Risk factors for low bone density include inadequate peak bone mass and excessive bone loss . In addition to the accelerated bone loss seen at the menopause, bone loss may also result from age-related conditions such as reduced calcium absorption from the gut and secondary hyperparathyroidism . In addition, certain medical and surgical conditions can produce so-called “secondary” osteoporosis. In the most comprehensive study to date, the Study of Osteoporotic Fractures , the determinants of BMD at various skeletal sites were assessed in a large number of Caucasian or Asian-American women aged 65 years or over, and included greater age at menopause, estrogen or thiazide use, non-insulin-dependent diabetes (NIDDM), and greater height, weight, strength and dietary calcium intake, all of which were positively associated with greater BMD at the distal radius. In contrast, older age, cigarette smoking, caffeine intake, prior gastric surgery and maternal history of fracture were negatively associated with BMD at that site (53). For the spine, greater weight, older age at menopause, a history of osteoarthritis, greater physical activity, moderate consumption of alcoholic beverages, treatment with diuretics and current HRT were associated with greater BMD, while later age at menarche and a maternal history of
fracture were associated with lower BMD . Increasing age positively correlated with spinal BMD in these elderly women, probably because of hypertrophic changes in the spine. Greater BMD of the femoral neck was positively associated with most of the same factors as those listed for the spine, together with quadriceps strength, calcium
intake, and a history of NIDDM . A history of maternal fracture and of prior wrist fracture was associated with low femoral neck BMD. Greater age was a risk factor for low BMD of the femoral neck, as it was for low BMD of the radius. Risk factors are reviewed in greater detail below.


Previous fracture
The occurrence of one osteoporotic fracture may increase the risk of future fractures. Thus in both men and women who have suffered a distal fracture of the forearm, the risk of subsequent fractures of the proximal femur and other skeletal sites is approximately doubled .

Genetics
Up to 50% of the variance in peak bone mass and some aspects of bone architecture and geometry relevant to bone strength may be determined genetically. . A family history of fragility fracture, and particularly of hip fracture, can be used in the risk assessment of patients .

Nutrition
Dietary factors influence peak bone mass, age-related bone loss and fracture risk. Calcium and vitamin D are particularly important since deficiencies are potentially correctable.


Calcium
The most consistent effects of calcium supplementation are observed in the appendicular skeleton, while effects on spinal bone appear to be transient. Older women seem to be more responsive to such supplementation than younger postmenopausal women. The relationship between calcium intake and fracture rate is less clear. While inverse correlations between dietary calcium intake and fracture (mainly of the hip) have been found in some studies, no significant correlation has been found in others and some have even shown a positive correlation between calcium intake and hip fracture. However, in a recent meta-analysis, it was reported that each additional gram of calcium in the diet was associated with a 25% reduction in hip fracture risk.

Vitamin D
Severe and prolonged deficiency of vitamin D results in rickets in children and osteomalacia in adults, conditions characterized by defective mineralization of bone. Osteomalacia will aggravate osteoporosis, since both increase the risk of fracture. Vitamin D deficiency is rare in Europe and the USA, but is still common in the Low levels of circulating vitamin D are common in elderly populations in many regions of the world and may contribute to fractures, particularly at the hip . A positive association between serum 1a,25-dihydroxycholecalciferol concentration and BMD was found in middle-aged and elderly women. Vitamin D supplementation prevents the reduction in BMD that occurs during the winter months in normal subjects.

Protein
Low protein intake is an important determinant of peak bone mass and therefore of the risk of osteoporosis in later life .The prevalence of malnutrition and undernutrition increase with advancing age and in patients with hip fracture. In the elderly, an association between low protein intake, low BMD and reduced mobility has been reported. This does not seem to be due to ageing itself, since healthy active elderly people and young adults are nutritionally not very different, in contrast to the acutely and chronically ill elderly population in whom signs of malnutrition are common . Undernutrition may increase the propensity to falls both by impairing coordination and reducing muscle strength. It is also an important determinant of the consequences of falling, since a reduction in the protective layer of soft tissue padding decreases the force required to fracture an osteoporotic hip.


Phosphate
A high dietary intake of phosphate in combination with a low intake of calcium increases serum PTH concentrations and may reduce BMD.

Vitamin K
Low plasma levels of vitamin K1 and K2 have been reported in patients with hip fracture. Vitamin K is essential for the production of gamma-carboxylated glutamyl residues present in several coagulation factors and bone proteins, particularly osteocalcin. Vitamin K deficiency can be assessed by measuring the undercarboxylated fraction of osteocalcin. This fraction increases with age and is therefore negatively related to BMD in elderly women. Undercarboxylated osteocalcin has been reported to be a predictor of hip fracture. However, protein–energy malnutrition is usually associated with multiple deficiencies so that the particular contribution of vitamin K deficiency to bone loss in undernourished patients sustaining hip fracture is unknown.


Magnesium and other trace elements and vitamins
Magnesium interferes with both the production and action of PTH, and thus indirectly affects bone metabolism. However, a specific role of magnesium in the maintenance of bone mass during adulthood has not yet been identified. Several trace elements are required for normal bone metabolism. Various animal and/or ecological studies in humans suggest that aluminum, boron, copper, fluoride, manganese, silicon, and zinc, as well as vitamins B6, B12 and C, may all play a protective role in the normal metabolism of bone tissue. Selective intervention studies are still required to identify their respective roles in the maintenance of bone mass, particularly in the elderly.


Physical inactivity
Immobility is an important cause of bone loss, and its detrimental effect on bone mass is far greater than the beneficial effect of additional exercise in an already ambulatory subject. Enforced immobility in healthy volunteers decreases bone mineral mass, as do motor deficits due to neurological disorders such as hemiplegia or paraplegia. Bone mineral mass also decreases during space flights despite vigorous physical exercise. In contrast, bone density increases in response to physical loading and mechanical stress. In many cross-sectional studies, a beneficial effect of weight-bearing exercise on peak bone mass has been reported. The observation that retired adult gymnasts have higher BMD than age-matched sedentary controls suggests the benefits of physical
activity outlast the termination of such activity, and the results of randomized controlled trials suggest that certain forms of exercise may retard bone loss. These studies also show that the skeletal site which is maximally loaded demonstrates the greatest effect. The type of loading also influences skeletal response.


Cigarette smoking
Definitely is definitely responsible for giving rise to a large number of diseases and this includes Osteoporosis as well. Smoke often kills the amount of calcium from the body of a person and this plays a significant role by giving rise to this disease. It is said that the weakness of the bones in many cases depends upon the factor that how much a person smoke in a day. Basically smoking is something that is considered as a calcium absorber as well as the killer of the tissues of the bones. The bone tissues are killed in a very large amount and when the tissues of the bones are killing the person’s face weak bone which is considered as Osteoporosis.

Alcohol consumption
Just like smoking alcohol also widely contributes in giving rise to this disease and this is considered as one of the primary reasons for the Osteoporosis in a large number of people. When a person takes alcohol on a regular basis he/she can get affected by the Osteoporosis very easily and in a very short period of time. Basically avoiding the alcohol is not easy for any person and it has been said that when a person fails in avoiding the alcohol on time probably he/she face this problem for a long period of time in the life.
It must be noted that because women have a weak bone density than men and also the bone density of older people are also less. This is the leading factor that is responsible for having the most number of cases of Osteoporosis in women.

Body mass index
Low body mass index (BMI) is associated with lower peak bone mass, and an adverse influence on bone loss . This may be the consequence of reduced peripheral estrogen production by adipose tissue among thin women, less mechanical loading of the skeleton, and metabolic influences on body composition. Excessive leanness is
also a risk factor for hip and vertebral fracture, and longitudinal epidemiological studies have shown that accelerated weight loss is an important determinant of the risk of hip fracture . In Europeans,
the risk of hip fracture is increased below a threshold BMI of 19kg/m2 . It is not known whether this threshold is also applicable to other populations.


Sex hormone deficiency
Primary hypogonadism in both sexes is associated with low bone mass, and decline in estrogen production at the menopause is the most important factor contributing to osteoporosis in later life. In addition, secondary amenorrhoea, as the result, e.g. of anorexia nervosa, excessive exercise or chronic disease, results in lower peak bone mass and increased risk of osteoporosis. Late menarche may be associated with lower peak bone mass and higher fracture risk. Finally, some studies indicate that the use of oral contraceptives may be associated with higher bone mass, although this finding has not been universal. A premature menopause, particularly
when surgically induced before age 45 years, is a strong determinant of bone density and increased risk of fracture.










COMMUNICATION BETWEEN OSTEOBLAST AND OSTEOCLAST

Communication between osteoblasts and osteoclasts


Osteoclast formation is controlled by several circulating hormones, including parathyroid hormone 1a,25-dihydroxycholecalciferol (calcitriol), and the gonadal steroids, estrogen and testosterone The microenvironment of the bone marrow also plays an essential role as a source of cytokines such as tumour necrosis factors (TNFs) and interleukins , which also regulate osteoclast formation and activity. These systemic and local factors regulate osteoclast formation and activity. Hormones and cytokines act on the osteoblastic lineage cells, which possess a cell surface molecule known as RANK ligand and a cell surface receptor, osteoprotegerin . RANKL is a member of the TNF ligand family that is present in osteoblastic lineage cells and interacts with osteoclast precursors from the haematopoietic lineage. This interaction promotes the differentiation and fusion of the osteoclast precursor, thus leading to the formation of mature osteoclasts. Osteoprotegerin is a soluble member of the TNF receptor superfamily that is produced by osteoblast lineage cells and inhibits osteoclast formation.


Mechanisms of Hormone Action.

Calcitonin inhibits bone resorption by acting directly on mature osteoclasts. Bisphosphonates, which are used in treating osteoporosis, also inhibit osteoclasts, probably by interfering with the system of communication between osteoblasts and osteoclasts. They also reduce the number of osteoclasts by inhibiting either their recruitment or their survival. Estrogen and probably testosterone exert their effects on the bone resorption by inhibiting the production of cytokines, particularly TNFs, interleukin-1 and interleukin-6.

Growth factors.
Osteoblast formation requires a transcription factor named cbfa1 osf2, which controls osteoblast differentiation and bone formation in the developing skeletons as well as the function of mature differentiated osteoblasts . Several growth factors, including insulin-like growth factors (IGFs), transforming growth factor-b, fibroblast growth factors, platelet-derived growth factor, bone morphogenetic proteins and prostaglandins can stimulate the proliferation of osteoblasts in vitro. Their respective importance in vivo is not yet clear. Nevertheless, it has been suggested that the production and action of growth factors are vital to the stimulation of bone formation in response to systemic hormones such as parathyroid hormone (PTH), osteogenic agents such as fluoride, and mechanical strain



Calcium homeostasis

Virtually all (99%) of the body’s calcium is located in bone and teeth. Only 0.1% is in the extracellular compartment and the remainder is within cells. The maintenance of a constant extracellular concentration of ionized calcium is essential, because calcium influences many physiological functions and biochemical pathways. The extracellular concentration of calcium is regulated by a dynamic equilibrium between the levels calcium in the intestine, kidney and bone . In young adults, the rates of calcium entering and leaving the extracellular compartment are equal. Net intestinal absorption of calcium corresponds to the difference between the amount of calcium absorbed and that diffusing from the extracellular compartment to the intestinal lumen. The urinary excretion of calcium represents the difference between the amount filtered and that reabsorbed. In a steady state, urinary calcium excretion corresponds roughly to the net calcium fluxes entering the extracellular compartment from the intestine and bone. In the kidney 98% of the calcium filtered by the glomerulus is reabsorbed in the renal tubule. The major regulator of the intestinal absorption of calcium is calcitriol, an active metabolite of vitamin D3 , which acts as a hormone. It is formed in the kidney, and its production is controlled by PTH, IGF-1, and the extracellular concentrations of calcium and phosphate . The main regulator of the tubular reabsorption of calcium is PTH, secretion of which is controlled by the extracellular concentration of calcium.

Gain of bone
Peak bone mass

The “peak bone mass” is the amount of bone tissue present at the end of skeletal maturation. It is a major determinant of the risk of fracture due to osteoporosis since the mass of bone tissue at any time during adult life is the difference between the amount accumulated at maturity and that lost with ageing. There is, therefore, considerable interest in exploring ways to increase peak bone mass. Epidemiological studies indicate a 10% increase in peak bone mass in the Caucasian female population would decrease the risk of hip fracture by about 30%. Such an increase would roughly correspond to the difference between male and female peak bone mass as measured at the radial or femoral diaphyseal site.


Measurement of bone mass

Most information in the characteristics of skeletal growth during childhood and adolescence has been obtained by non-invasive techniques that enable bone mass to be measured at various sites in the skeleton with great precision and accuracy. The bone mass of a particular part of the skeleton is directly dependent on both the volume or size of the part concerned and the density of the mineralized tissue contained within its periosteal envelope. The mean volumetric mineral density of bony tissue (in g of hydroxyapatite per cm3) can be determined non-invasively by quantitative computed tomography (QCT) . The so-called “areal” or “surface” bone mineral density can be determined by single- or dual-energy X-ray absorptiometry (SXA and DXA). The values generated by these techniques are directly dependent on both the size and integrated mineral density of the scanned skeletal tissue. The integrated mineral density is determined by cortical thickness, the number and thickness of the trabeculae, and the “true” mineral density corresponding to the amount of hydroxyapatite per unit volume of the bone organic matrix.

Development of bone mass

There is no evidence for sex differences in bone mass of either the axial or appendicular skeleton at birth. Similarly, the volumetric BMD appears to be the same in female and male newborns. This absence of a substantial sex difference in bone mass is maintained until the onset of puberty . The difference following puberty is characterized by a more prolonged period of bone maturation in males than in females, resulting in a greater increase in bone size and cortical thickness. Puberty has a much greater effect on bone size than on the volumetric mineral density . There is no significant sex difference in the volumetric trabecular density at the end of puberty. During puberty, the rate of accumulation of BMD at both the lumbar spine and femoral neck increases 4–6-fold over a 3- and 4-year period in females and males, respectively. The rate of increase in bone mass is less marked in the disphysis of long bones than elsewhere. There is an asynchrony between the gain in standing height and the growth of bone mineral mass during puberty. This phenomenon may be responsible for the transient fragility that may contribute to the higher incidence of fracture that occurs near puberty when the dissociation between the rate of statural growth and mineral mass accrual is maximal.



Endocrine factors and calcium phosphate metabolism during growth
Various endocrine factors, including gonadal sex hormones and adrenal androgens (dehydroepiandrosterone and androstenedione) influence bone growth. The production of these steroids increases before and during puberty, but the time-course of their production does not match the accelerated gain in bone mass. In contrast, IGF-1 and
calcitriol concentrations and the tubular reabsorption of inorganic phosphate and plasma phosphate rise with the accrual of bone mass. This may be an adaptive response to the increased demand for calcium
and phosphate.

External factors
Modification of environmental factors can cause an individual to change the track of bone accrual. Nutritional factors are particularly important determinants of peak bone mass and rate of gain of bone mass. In addition to the non-specific influence of caloric intake, both experimental and clinical evidence indicate that the amount of calcium and protein in the diet modulate the gain in bone mass. Several intervention studies report that calcium supplementation significantly enhances the rate of BMD in children andadolescents . The role of physical activity is discussed later. Interactions between environmental factors such as dietary intake and physical exercise, as well as between genetic and environmental factors, might play an important role in the acquisition of bone mineral mass. Some data suggest that the magnitude of the bone response to calcium supplementation in prepubertal children varies according to the genotype of the vitamin D receptor .

Loss of bone
The onset of substantial bone loss is usually around age 65 years in men and 50 years in women . Nevertheless, even in the absence of risk factors, some bone loss can be detected before the menopause at certain skeletal sites. Indeed, a decrease in BMD of the proximal femur has been described in the third decade. There is little variation
in bone size throughout life, beyond continuous, slight expansion of the outer dimensions. This phenomenon is more marked in men than in women, and affects both the axial and the peripheral skeleton . The expansion of the periosteal surface is less than the increase in space occupied by the bone marrow which results from a greater
resorption at the endosteal surface. Under these conditions, the bone cortex becomes thinner. This process, together with increasing porosity of cortical bone and destruction of trabeculae through thinning and perforation, accounts for age-dependent bone loss.

Endocrine factors

Estrogen deficiency
Estrogen is necessary, not only for maximizing peak bone mass in men and women, but also for maintaining it. It controls bone remodelling in reproductively active women and in ageing men. Even a shortening of the luteal phase may be associated with abnormal bone in women . Estrogen deficiency and low bone mass also result from conditions such as anorexia nervosa, or exercise- induced amenorrhoea, or from the use of substances that inhibit gonadotropin secretion . Estrogen deficiency accelerates the rate of bone turnover, thereby altering the balance between bone formation and bone resorption, and appears to be the main cause of osteoporosis in women after the fifth decade, and possibly in men. It is thus directly implicated in the age-related increase in the incidence of fragility fractures . It is now clearly established that the rate of bone loss does not decrease with age, but continues throughout the whole of life, at least at peripheral skeletal sites.


Several cytokines released in the bone marrow increase the rate of bone turnover . TNF-a, interleukin-1 and interleukin-6, all stimulate bone resorption in vitro and in vivo, and may initiate the bone loss induced by estrogen deficiency. In a study using the transgenic mouse model in which the activity of TNF-a was permanently prevented by the presence of high levels of circulating soluble TNF-a receptor 1 (24), no decrease in bone mass or increase in bone turnover was observed after oophorectomy in transgenic mice when compared with control mice, suggesting a key role for TNF-a. While there is evidence that TNF-a, interleukin-1 and interleukin-6 are all involved in bone remodelling and show a considerable degree of interplay, only TNF-a appears to be required for the enhanced bone remodelling that occurs after estrogen depletion. This evidence is also consistent with the role of osteoprotegerin, an inhibitor of osteoclast formation. As osteoprotegerin is a soluble member of the TNF receptor superfamily, it has the capacity to neutralize the activity of TNF on osteoclastogenesis.


Other endocrine causes of bone loss
In addition to gonadal deficiency, which is an important cause of osteoporosis in men, other endocrine diseases can also cause bone loss by affecting the remodelling of bone . Primary hyperparathyroidism and hyperthyroidism increase the rate of bone turnover, thereby inducing bone loss . In contrast, excess glucocorticoids reduce bone formation. In addition, administration of glucocorticoids in pharmacological excess may decrease the intestinal absorption of calcium and possibly also its reabsorption by the renal tubules. These latter two effects would lead to a negative calcium balance and result in increased bone resorption through a mechanism which may include secondary hyperparathyroidism . Daily doses of 7.5 mg of prednisolone are sufficient to induce skeletal losses.