Category Archives: Diet

Coconut Oil Reduces Oxidative Stress of Bone in Rats

Abstract

The effects of virgin coconut oil on bone oxidative status in ovariectomised rat.

Virgin coconut oil (VCO) was found to have antioxidant property due to its high polyphenol content. The aim of this study was to investigate the effect of the virgin coconut oil on lipid peroxidation in the bone of an osteoporotic rat model. Normal female Sprague-Dawley rats aged 3 months old were randomly divided into 4 groups, with 8 rats in each group: baseline, sham, ovariectomised (OVX) control group, and OVX given 8% VCO in the diet for six weeks. The oxidative status of the bone was assessed by measuring the index of lipid peroxidation, which is malondialdehyde (MDA) concentration, as well as the endogenous antioxidant enzymes glutathione peroxidase (GPX) and superoxide dismutase (SOD) in the tibia at the end of the study. The results showed that there was a significant decrease in MDA levels in the OVX-VCO group compared to control group. Ovariectomised rats treated with VCO also had significantly higher GPX concentration. The SOD level seemed to be increased in the OVX-VCO group compared to OVX-control group. In conclusion, VCO prevented lipid peroxidation and increased the antioxidant enzymes in the osteoporotic rat model.

Abujazia MA, Muhammad N, Shuid AN, Soelaiman IN
Evid Based Complement Alternat Med 2012
PMID: 22927879 | Free Full Text

This is significant for bone strength because:

Increased activity of reactive oxygen species (ROS) leads to overexpressions of TNF-α, RANKL, and M-CSF which enhance osteoclasts function and induce bone loss [7, 8]. Oxidative stress also suppresses bone formation by inhibiting osteoblast differentiation and decreasing the survival of these cells [9, 10].

Coconut Oil Increases Bone Strength in Rats

Abstract

Effect of consumption of fatty acids, calcium, vitamin D and boron with regular physical activity on bone mechanical properties and corresponding metabolic hormones in rats.

The consumption of fatty acids, nutrients, and regular physical activity, individually influence bone mechanical properties in rats. To investigate their effects in combination, male rats were divided into the seven groups: G1: regular food and drinking water; G2: same as Gr.1 + physical activity (Whole body vibration; WBV); G3: same as Gr.2 + Calcium, Vit. D, Boron; G4: same as Gr.3 + canola oil; G5: same as Gr.3 + sunflower oil; G6: same as Gr.3 + mix of sunflower oil and canola oil; and G7: same as Gr.3 + coconut oil; and treated for 8 weeks. Analysis between the control with the groups 2 and 3 revealed that vibration in the G2 increased the body weight (P = 0.04), with no other major difference in plasma and bone indices. Comparison between the control with the G4-G7 (the oil groups) revealed that the rats in the G5 had a lower body weight (15 % less) and a significant increase in plasma levels of Estradiol in the G7 was noted. In addition, levels of Testosterone in the G4 and G7, and Free Testosterone in the G7 had a remarkable increase. Similar trend was observed for plasma levels of Vit. D in the G4 and G5. The stiffness and the breaking strength of the femur in the G7, and the breaking strength of the lumbar in the G7 compared to the control and the G4 and G5 was significantly higher and tended to increase in comparison to the G6. Better and stronger measurements observed for coconut oil is warranted to further study its effect on biomechanical properties of bones.

Naghii MR, Ebrahimpour Y, Darvishi P, Ghanizadeh G…
Indian J. Exp. Biol. Mar 2012
PMID: 22439438

Exercise Limits Effects of Excessive Alcohol on Bone in Rats

Abstract

Regular exercise limits alcohol effects on trabecular, cortical thickness and porosity, and osteocyte apoptosis in the rat.

Excessive alcohol consumption is known to be a cause of secondary osteoporosis whereas physical activity is recommended in prevention of osteoporosis. This study was designed to analyze the effects of physical exercise on bone parameters in chronic alcohol-fed rats.
Forty-eight male Wistar rats were divided in four groups: Control (C), Alcohol (A), Exercise (E) and Alcohol+Exercise (AE). A and AE groups drank a solution composed of ethanol and water (35% volume/volume for 17 weeks). E and AE groups were submitted to treadmill training for 14 weeks (60 min/day, 5 times/week). Bone mineral density (BMD) was assessed by DXA, the trabecular and cortical microarchitectural parameters by microCT and serum osteocalcin, NTx and leptin concentrations by ELISA assays. Bone mechanical parameters were evaluated through mechanical testing. Osteocyte apoptosis was analyzed with cleaved caspase-3 immunostaining.
Alcohol-fed rats had significantly lower body weight (-28%), fat (-46%) and lean mass (-25%) compared to controls. BMD (-8%), trabecular (-12%) and cortical thickness (-27%) were significantly lower with alcohol whereas porosity (+38%) and pore number (+42%) were higher. Exercise combined with alcohol prevented lower Tb.Th (+20%), Ct.Th (+30%), stress (+26%) and higher Ct.Po (-24%) and osteocyte apoptosis (-91%) compared to A. However, WB BMD (-4%) and femur BMD were still lower in AE versus C.
Regular physical activity has beneficial effects on some microarchitectural parameters in alcohol-fed rats. However, regular treadmill exercise does not compensate for the effects of heavy chronic alcohol consumption on whole body bone density.

Maurel DB, Boisseau N, Pallu S, Rochefort GY…
Joint Bone Spine Oct 2013
PMID: 23380443

Alcohol Reduces Bone Resorption Markers

Abstract

Moderate ingestion of alcohol is associated with acute ethanol-induced suppression of circulating CTX in a PTH-independent fashion.

The “J shape” curve linking the risk of poor bone health to alcohol intake is now well recognized from epidemiological studies. Ethanol and nonethanol components of alcoholic beverages could influence bone remodeling. However, in the absence of a solid underlying mechanism, the positive association between moderate alcoholic intake and BMD remains questionable because of confounding associated social factors. The objective of this work was to characterize the short-term effects of moderate alcohol consumption on circulating bone markers, especially those involved in bone resorption. Two sequential blood-sampling studies were undertaken in fasted healthy volunteers (age, 20-47 yr) over a 6-h period using beer of different alcohol levels (<0.05-4.6%), solutions of ethanol or orthosilicic acid (two major components of beer), and water +/- calcium chloride (positive and negative controls, respectively). Study 1 (24 subjects) assessed the effects of the different solutions, whereas study 2 (26 subjects) focused on ethanol/beer dose. Using all data in a “mixed effect model,” we identified the contributions of the individual components of beer, namely ethanol, energy, low-dose calcium, and high-dose orthosilicic acid, on acute bone resorption. Markers of bone formation were unchanged throughout the study for all solutions investigated. In contrast, the bone resorption marker, serum carboxy terminal telopeptide of type I collagen (CTX), was significantly reduced after ingestion of a 0.6 liters of ethanol solution (>2% ethanol; p <or= 0.01, RM-ANOVA), 0.6 liters of beer (<0.05-4.6% ethanol; p < 0.02), or a solution of calcium (180 mg calcium; p < 0.001), but only after calcium ingestion was the reduction in CTX preceded by a significant fall in serum PTH (p < 0.001). Orthosilicic acid had no acute effect. Similar reductions in CTX, from baseline, were measured in urine after ingestion of the test solutions; however, the biological variability in urine CTX was greater compared with serum CTX. Modeling indicated that the major, acute suppressive effects of moderate beer ingestion (0.6 liters) on CTX were caused by energy intake in the early phase (approximately 0-3 h) and a “nonenergy” ethanol component in the later phase (approximately 3 to >6 h). The early effect on bone resorption is well described after the intake of energy, mediated by glucagon-like peptide-2, but the late effect of moderate alcohol ingestion is novel, seems to be ethanol specific, and is mediated in a non-calcitonin- and a non-PTH-dependent fashion, thus providing a mechanism for the positive association between moderate alcohol ingestion and BMD.

Sripanyakorn S, Jugdaohsingh R, Mander A, Davidson SL…
J. Bone Miner. Res. Aug 2009
PMID: 19257829 | Free Full Text

Garlic Oil Prevents Bone Loss in Ovariectomized Rats

Abstract

Role of peritoneal macrophages and lymphocytes in the development of hypogonadal osteoporosis in an ovariectomized rat model: possible phytoestrogenic efficacy of oil extract of garlic to preserve skeletal health.

This study was to examine whether skeletal health deterioration in the hypogonadal situation is a consequence of an alteration in the functional status of peripheral mononuclear cells and its amelioration, if any, by an oil extract of garlic. The results suggest that hypogonadism-induced oxidative stress of peritoneal macrophages and lymphocytes could be reduced by supplementation with an oil extract of garlic. However, estrogen deficiency did not cause any significant change in DNA fragmentation of peritoneal macrophages. The hypogonadism-induced increase in the serum levels of IL-6 and TNF-alpha were significantly reduced by an oil extract of garlic. Further, such supplementation could revive the hypogonadism-induced decrease in serum estrogen titer and counter-balance the increase in bone turnover as determined by low bone tensile strength and alterations in bone related biochemical variables such as urinary calcium, hydroxyproline, calcium to creatinine ratio and serum tartrate resistant acid phosphatase activity (TRAP). The garlic oil supplemented partial recovery of the serum estrogen titer in hypogonadal rats was found to be persistently associated with reduced oxidative stress of peritoneal macrophages and lymphocytes, reduced serum interleukins and better preservation of bone mass. This study proposes that the hypogonadism-induced bone loss has a direct correlation with the functional status of lymphocytes and peritoneal macrophages, and garlic can prevent this.

Mukherjee M, Das AS, Das D, Mukherjee S…
Phytother Res Nov 2007
PMID: 17600860

Garlic Oil Prevents Bone Mineral Loss in Rats

Abstract

Role of oil extract of garlic (Allium sativum Linn.) on intestinal transference of calcium and its possible correlation with preservation of skeletal health in an ovariectomized rat model of osteoporosis.

The present study was undertaken to examine the effects of an oil extract of garlic on the in vivo intestinal transference of calcium, and also to verify its role in maintaining the bone mineral content and bone tensile strength in an ovariectomized rat model of osteoporosis. The results suggest that, in this experimental model, oil extract of garlic promotes intestinal transference of calcium by modulating the activities of both intestinal alkaline phosphatase and Ca(2+) activated ATPase. Also the observed low bone mineral content and low bone tensile strength in these rats were significantly restored by garlic oil supplementation. Further, garlic oil supplementation was able to revive partially the bilateral ovariectomy-induced decrease in the serum estrogen titer. The serum parathyroid hormone level, however, was found unaltered in these rats. The garlic oil supplemented partial recovery in serum estrogen titer in bilaterally ovariectomized rat was found to be persistently associated with enhanced calcium transference and better preservation of bone mineral content. The results of this study propose that the phytoestrogenic efficacy of an oil extract of garlic prevents ovarian hormone deficiency induced bone mineral loss possibly by promoting intestinal transference of calcium through the partial revival of the serum estrogen titer.

Mukherjee M, Das AS, Das D, Mukherjee S…
Phytother Res May 2006
PMID: 16619371

Garlic < Lovastatin < Estrogen Effective in suppressing Bone loss in Ovariectomized Rats

Abstract

Effects of garlic oil on postmenopausal osteoporosis using ovariectomized rats: comparison with the effects of lovastatin and 17beta-estradiol.

The purpose of this study was to examine the antiosteoporosis effects of garlic oil in an ovariectomized (Ovx) rat model of osteoporosis and to compare its efficacy with lovastatin (a synthetic hypocholesterolemic drug) and 17beta-estradiol (a potent antiosteoporotic agent). Animals were divided into five groups: sham-operated control, ovariectomized, ovariectomized supplemented with lovastatin, ovariectomized supplemented with garlic oil and ovariectomized supplemented with 17beta-estradiol. In our study, the development of a high rate of bone turnover and osteoporosis in the ovariectomized animals were confirmed by significant alterations of serum alkaline phosphatase activity, serum tartrate-resistant acid phosphatase activity, urinary excretion of calcium, phosphate, hydroxyproline and urinary calcium to creatinine ratio, when compared with the sham-operated control group. Supplementation of these animals with either garlic oil or lovastatin or 17beta-estradiol, in addition to their hypocholesterolemic effect, could counterbalance all these changes. The results revealed that all three compounds significantly protected the hypogonadal bone loss as reflected by higher bone densities and higher bone mineral contents than the ovariectomized group of animals. The results emphasize that, like 17beta-estradiol, the hypocholesterolemic compounds garlic oil and lovastatin are also effective in suppressing bone loss owing to estrogen deficiency and their efficacy in the order of lower to higher is garlic < lovastatin < 17beta-estradiol.

Mukherjee M, Das AS, Das D, Mukherjee S…
Phytother Res Jan 2006
PMID: 16397916

Garlic Oil Reverses Bone Loss in Ovariectomized Rats

Abstract

Prevention of bone loss by oil extract of garlic (Allium sativum Linn.) in an ovariectomized rat model of osteoporosis.

The effects of oil extract of garlic (Allium sativum Linn.) on different primary and secondary osteoporotic marker changes were tested in an ovariectomized rat model of osteoporosis. Experiments were performed on three different rat models: sham-operated control, ovariectomized and ovariectomized supplemented with garlic oil. In ovariectomized group, there has been a significant increase in different relative organ weights compared to sham-operated control, while the uterine weight was found to be decreased. Supplementation with oil extract of garlic could effectively reverse these changes. Also low bone densities that developed in the ovariectomized group were significantly recovered in the garlic oil supplemented group. In our study, the development of high rate of bone turnover and osteoporosis in the ovariectomized animals were confirmed by significant alteration of serum alkaline phosphatase activity, serum tartrate resistant acid phosphatase activity, urinary excretion of calcium, phosphate, hydroxyproline and urinary calcium to creatinine ratio, when compared with the sham-operated control group. Garlic oil extract supplementation, apart from its unique influence in lowering blood cholesterol, could also prevent ovariectomy-induced rise in all the above-mentioned marker changes. The results of this study emphasize that oil extract of garlic possibly has a positive role in suppressing ovariectomy-induced bone resorption.

Mukherjee M, Das AS, Mitra S, Mitra C
Phytother Res May 2004
PMID: 15173999

Zinc Deficiency or Calorie Restriction Impares Bone Development in Weanling Rats

Abstract

Zinc-deficient rats have more limited bone recovery during repletion than diet-restricted rats.

The objective of this study was to investigate the effects of dietary zinc deficiency and diet restriction on bone development in growing rats, and to determine whether any adverse effects could be reversed by dietary repletion. Weanling rats were fed either a zinc-deficient diet ad libitum (ZD; <1 mg zinc/kg) or nutritionally complete diet (30 mg zinc/kg) either ad libitum (CTL) or pair-fed to the intake of the ZD group (DR; diet-restricted) for 3 weeks (deficiency phase) and then all groups were fed the zinc-adequate diet ad libitum for 3, 7, or 23 days (repletion phase). Excised femurs were analyzed for bone mineral density (BMD) using dual-energy x-ray absorptiometry, and plasma was analyzed for markers of bone formation (osteocalcin) and resorption (Ratlaps). After the deficiency phase, ZD had lower body weight and reduced femur BMD, zinc, and phosphorus concentrations compared with DR; and these parameters were lower in DR compared with CTL. Femur calcium concentrations were unchanged among the groups. Reduced plasma osteocalcin in ZD and elevated plasma Ratlaps in DR suggested that zinc deficiency limits bone formation while diet restriction accelerates bone resorption activity. After 23 days of repletion, femur size, BMD, and zinc concentrations remained lower in ZD compared with DR and CTL. Body weight and femur phosphorus concentrations remained lower in both ZD and DR compared with CTL after repletion. There were no differences in plasma osteocalcin concentrations after the repletion phase, but the plasma Ratlaps concentrations remained elevated in DR compared with CTL. In summary, both ZD and DR lead to osteopenia during rapid growth, but the mechanisms appear to be due to reduced modeling in ZD and higher turnover in DR. Zinc deficiency was associated with a greater impairment in bone development than diet restriction, and both deficiencies limited bone recovery during repletion in growing rats.

Hosea HJ, Taylor CG, Wood T, Mollard R…
Exp. Biol. Med. (Maywood) Apr 2004
PMID: 15044713

Review: Alkaline Diets and the Acid Load Theory are Bunk – 2013

Abstract

Nutritional disturbance in acid-base balance and osteoporosis: a hypothesis that disregards the essential homeostatic role of the kidney.

The nutritional acid load hypothesis of osteoporosis is reviewed from its historical origin to most recent studies with particular attention to the essential but overlooked role of the kidney in acid-base homeostasis. This hypothesis posits that foods associated with an increased urinary acid excretion are deleterious for the skeleton, leading to osteoporosis and enhanced fragility fracture risk. Conversely, foods generating neutral or alkaline urine would favour bone growth and Ca balance, prevent bone loss and reduce osteoporotic fracture risk. This theory currently influences nutrition research, dietary recommendations and the marketing of alkaline salt products or medications meant to optimise bone health and prevent osteoporosis. It stemmed from classic investigations in patients suffering from chronic kidney diseases (CKD) conducted in the 1960s. Accordingly, in CKD, bone mineral mobilisation would serve as a buffer system to acid accumulation. This interpretation was later questioned on both theoretical and experimental grounds. Notwithstanding this questionable role of bone mineral in systemic acid-base equilibrium, not only in CKD but even more in the absence of renal impairment, it is postulated that, in healthy individuals, foods, particularly those containing animal protein, would induce ‘latent’ acidosis and result, in the long run, in osteoporosis. Thus, a questionable interpretation of data from patients with CKD and the subsequent extrapolation to healthy subjects converted a hypothesis into nutritional recommendations for the prevention of osteoporosis. In a historical perspective, the present review dissects out speculation from experimental facts and emphasises the essential role of the renal tubule in systemic acid-base and Ca homeostasis.

Bonjour JP
Br. J. Nutr. Oct 2013
PMID: 23551968 | Free Full Text

…experiments carried out among patients suffering from severe metabolic acidosis caused by renal insufficiency, or among healthy subjects made acidotic by administering NH4Cl, suggested the involvement of bone tissue in maintaining the acid–base balance. This hypothesis was later refuted on the basis of both theoretical and experimental arguments. Despite this rebuttal, the hypothesis was put forward that bone could play a buffering role, with the consideration that nutrients, particularly animal proteins with their acid load, could be a major cause of osteoporosis. Several recent human studies have shown that there is no relationship between nutritionally induced variations of urinary acid excretion and Ca balance, bone metabolism and the risk of osteoporotic fractures. Variations in human diets across a plausible range of intakes have been shown to have no effect on blood pH. Consistent with this lack of a mechanistic basis, long-term studies of alkalinising diets have shown no effect on the age-related change in bone fragility. Consequently, advocating the consumption of alkalinising foods or supplements and/or removing animal protein from the human diet is not justified by the evidence accumulated over the last several decades.