Clinical Nutrients for Osteoporosis

 

Good Evening!

Clinical Nutrients for Osteoporosis
by Tori Hudson, ND

Numerous modifiable and non-modifiable factors influence the risk of developing
osteoporosis. This article provides the practitioner with an understanding of
supplementary clinical nutrients and their effect on bone loss and fractures.
Lifestyle modifications and nutrient supplementation may be able to reduce the
risk of osteoporosis and the associated debilitating fractures. For women who
have already been diagnosed with osteoporosis, these nutritional factors can
serve as an adjunct to conventional therapies to slow bone loss and, more
importantly, decrease the risk of fractures.

NUTRITIONAL SUPPLEMENTATION

Calcium
Adequate calcium intake has an established role in maintaining bone health,
primarily in very young women and the elderly. However, calcium is only modestly
effective for slowing the loss of bone mineral density in peri- and early
postmenopausal women. Calcium supplementation also appears to have an important
role in improving the efficacy of pharmaceutical agents used to treat bone loss
and osteoporosis.

Prior to the Women's Health Initiative study, there was no clear evidence that
higher calcium intake decreased fracture risk.1 A meta-analysis of prospective
cohort studies and clinical trials found that higher calcium intake and calcium
supplementation were not associated with a lower incidence of hip fractures.2 In
a 2004 meta-analysis of randomized controlled trials, supplementation with
500-2,000 mg per day of calcium had only a modest benefit on bone density in
postmenopausal women: the difference in the amount of bone loss between calcium
and placebo was 2.05% for the total body, 1.66% for the lumbar spine, and 1.64%
for the hip.3 Two trials within this meta-analysis suggested a modest and
nonsignificant benefit with calcium supplementation and the risk of nonvertebral
fractures. In the Women's Health Initiative, which enrolled more than 36,000
postmenopausal women, supplementation with 1,000 mg per day of calcium and 400
IU per day of vitamin D decreased the risk of hip fractures nonsignificantly by
12%, when compared with placebo. However, when the analysis was restricted to
women who took the tablets at least 80% of the time, calcium plus vitamin D
significantly decreased hip fractures by 29% compared with placebo.4

Other calcium studies also showed a beneficial effect on bone loss. In
postmenopausal women, calcium supplementation has been shown to decrease bone
loss by as much as 50% at nonvertebral sites. The effects were greatest in women
whose baseline calcium intake was low, in older women, and in women with
established osteoporosis.5 In a study by Elders et al,6 a significant decrease
in vertebral bone loss was observed with supplementation of 1,000 to 2,000 mg
per day of calcium for 1 year. Bone loss was also less in the calcium group than
in the control group after 2 years, but the difference was no longer
statistically significant.

Dietary calcium is essential throughout a woman's life, and requirements
increase with advancing age, in part due to reduced calcium absorption and
decreased renal calcium conservation. However, calcium supplementation by itself
is not effective in preventing the accelerated bone loss that occurs in the
first few years after menopause. Ten years postmenopausally, calcium
supplementation again becomes effective in reducing age-related bone loss.7
While consuming an adequate amount of calcium is important, it is too often
overemphasized, supplemented at excessive doses, and is only one of many
nutritional and lifestyle factors that play a role in promoting bone health.

Vitamin D
Vitamin D enhances intestinal calcium absorption, thereby contributing to a
favorable calcium balance in the body. Increased calcium absorption also reduces
parathyroid-hormone-mediated bone resorption. In the United States, most infants
and young children have adequate vitamin D consumption from fortified milk.
During adolescence, however, the consumption of dairy products drops off, and
inadequate vitamin D intake is more likely to adversely affect calcium
absorption.

Several large randomized controlled trials have found that the combination of
calcium and vitamin D had no significant effect on fracture risk.1,8,5

However, a meta-analysis of randomized controlled trials in elderly
postmenopausal women found that a dose of 700 – 800 IU per day of vitamin D was
associated with significant reductions in the risk of hip and nonvertebral
fractures.9 Especially in older women, vitamin D in combination with calcium
supplementation reduced the rate of postmenopausal bone loss.10 Vitamin D has
also been shown to improve muscle strength11 and balance12, thereby reducing the
risk of falling.13

Magnesium
Magnesium is a cofactor for alkaline phosphatase, which plays a role in bone
mineralization. Low magnesium status is common in women with osteoporosis, and
magnesium deficiency is associated with abnormal bone mineral crystals.14 Some
women with reduced bone mineral density do not have an increased fracture rate,
possibly because their bone mineral crystals are of high quality, due in part to
high levels of magnesium. In a group of postmenopausal women, supplementation
with 250-750 mg per day of magnesium for 6 months, followed by 250 mg per day
for 6-18 months, resulted in an increase in bone density in 71% of women. This
increase was noteworthy, because it occurred without calcium supplementation.15

Strontium
Strontium is a non-radioactive earth element physically and chemically similar
to calcium. Strontium ranelate is the specific strontium salt used in clinical
trials for osteoporosis, but this form of strontium is not available in the U.S.
Strontium in large doses stimulates bone formation and reduces bone resorption.
In a phase 2 clinical trial, 2 g per day of oral strontium ranelate (containing
680 mg per day of elemental strontium) for three years was shown to reduce the
risk of vertebral fractures and to increase bone mineral density in 1,649
postmenopausal women with osteoporosis.16

In the first year, there was a 49% reduction in the incidence of vertebral
fractures in the strontium ranelate group and 41% reduction at the end of three
years. After adjusting for artifact effect on imaging, a 6.8% increase in bone
mineral density was seen at the lumbar spine after 3 years of strontium
supplementation.. There was also an 8.3% increase at the femoral neck, but there
was insufficient data to adjust it for an artifact effect, and therefore it is
not clear as to how accurate this is.
In a two year trial 353 postmenopausal women with osteoporosis and a history of
at least one vertebral fracture received a placebo or one of three different
doses of strontium: 170 mg per day, 340 mg per day or 680 mg per day.17 A small
increase in lumbar bone mineral density was seen with each dose of strontium,
but the difference compared with placebo was statistically significant only for
the highest dose. The incidence of new vertebral fractures was lowest (38.8%)
with the lowest dose of strontium, vs. 54.7%, 56.7% and 42.0% in the placebo,
340 mg per day and 680 mg per day groups, respectively.

Strontium chloride is the most common form of strontium used in U.S.
supplements. This form of strontium has not been the subject of published
research. Due to potential adverse effects of higher doses of strontium,
including rickets, bone mineralization defects, and interference with vitamin D
metabolism, it may be prudent to use low doses until more research is conducted.

Zinc
Zinc is essential for the formation of osteoblasts and osteoclasts, and it
enhances the biochemical action of vitamin D. Zinc is also is necessary for the
synthesis of various proteins found in bone. Low zinc levels have been found in
the serum and bone of elderly people with osteoporosis.18

Copper
A deficiency of copper is known to produce abnormal bone development in growing
children, and may be a contributing cause of osteoporosis. In vitro studies have
shown that copper supplementation inhibits bone resorption.19,20 In a
double-blind trial, supplementation with 3 mg per day of copper for 2 years
significantly decreased bone loss in postmenopausal women.21

Manganese
A deficiency of manganese may be one of the lesser known but more important
nutritional factors related to osteoporosis. Manganese deficiency causes a
reduction in calcium deposition in bone. Manganese also stimulates
mucopolysaccharide production, which provides a framework for the calcification
process.22

Zinc, Copper, and Manganese
In a double-blind study of postmenopausal women, the combination of zinc,
copper, manganese, and calcium appeared to be more effective than calcium alone
for preventing bone loss in postmenopausal women.23

Boron
Boron supplementation reduces urinary excretion of calcium and magnesium and
increases serum levels of 17beta-estradiol and testosterone in postmenopausal
women.24 These observations suggest that boron supplementation could help
prevent bone loss.

Silicon
During bone growth and the early phases of bone calcification, silicon has an
essential role in the formation of cross-links between collagen and
proteoglycans. In animals, silicon-deficient diets have produced abnormal skull
development and growth retardation,25 and supplemental silicon partially
prevented trabecular bone loss in ovariectomized rats.26

Other Nutritional Factors

Folic Acid and Vitamin B12
Accelerated bone loss in menopausal women may in part be due to increased levels
of homocysteine, a breakdown product of methionine. Homocysteine has the
potential to promote osteoporosis if it is not eliminated adequately. In a
prospective study, women with high homocysteine levels had almost twice the risk
of nonvertebral osteoporotic fractures as did women with low homocysteine
levels. There was no association in that study between homocysteine levels and
bone mineral density at either the femoral neck or the lumbar spine, which
suggests that the reduction in fracture risk was due to an improvement in bone
quality.27 Folic acid promotes the remethylation of homocysteine to methionine,
and supplementing postmenopausal women with this nutrient results in significant
reductions in homocysteine levels. Vitamin B12 has also been shown to reduce
homocysteine levels.28 In a double-blind study of stroke victims with elevated
homocysteine levels, daily supplementation with 5 mg of folic acid plus 1,500
mcg of vitamin B12 for two years reduced hip fracture incidence by 78%, compared
with placebo.29

Vitamin B6
Vitamin B6 also plays a role in homocysteine metabolism. In people with the
genetic disorder homocystinuria, vitamin B6 supplementation reverses the
elevated levels of homocysteine.30 Animal studies have shown that vitamin B6
deficiency can prolong fracture healing time,31 impair cartilage growth, cause
defective bone formation,32 and promote osteoporosis.33 Vitamin B6 may also
influence progesterone production and exert a synergistic effect on
estrogen-sensitive tissue. Laboratory evidence of low vitamin B6 status appears
to be common, even among healthy individuals.34

Vitamin C
Vitamin C promotes the formation and cross-linking of some of the structural
proteins in bone. Animal studies have shown that vitamin C deficiency can cause
osteoporosis35 and it has been known for decades that scurvy, a disease caused
by vitamin C deficiency, is also associated with abnormalities of bone.

Vitamin K
Vitamin K is required for the production of the bone protein, osteocalcin.
Osteocalcin draws calcium to bone tissue, enabling calcium crystal formation.
Osteocalcin provides the protein matrix for mineralization and is thought to act
as a regulator of bone mineralization.36 Vitamin K plays a key role in the
formation, remodeling, and repair of bone by attracting calcium to the site of
this protein matrix.37 A low dietary intake of vitamin K seems to increase the
risk of osteoporotic hip fractures in women, according to data from the Nurses'
Health Study.38

There are various forms of vitamin K, but the human trials have been done on
vitamin K1 (phylloquinone) and menaquinone-4, (MK4, a form of vitamin K2).

In a double-blind study, 452 men and women (ages 60-80 years) received a
multiple vitamin/mineral supplement that provided 600 mg per day of calcium and
400 IU per day of vitamin D, plus either 500 mcg per day of vitamin K1 or no
vitamin K1.39 Bone mineral density (determined by dual-energy x-ray
absorptiometry) and bone turnover were measured at 6, 12, 24 and 36 months.
There were no differences in bone mineral density at the femoral neck, lumbar
spine, or total body, between the two treatment groups, indicating that vitamin
K1 did not enhance the effects of calcium, vitamin D, and other nutrients in
this patient population. In the double-blind ECKO trial,40 a daily 5-mg
supplement of vitamin K1 for 2 to 4 years did not protect against age-related
decline in bone mineral density in postmenopausal women with osteopenia, but
significantly fewer women in the vitamin K group than in the placebo group had
fractures.

Epidemiological evidence has shown associations between low dietary intake of
vitamin K and increased bone loss in elderly men and women. A 2006 meta-analysis
of 13 randomized controlled trials41 that gave vitamin K1 or menaquinone-4 (a
form of vitamin K2) supplements for longer than 6 months reported data on bone
loss and fracture rates. All but one study showed a reduction in bone loss with
supplemental vitamin K. All 7 of the 13 studies that reported fracture data were
in Japanese individuals and used menaquinone-4. Most of these trials used a high
dose, 45 mg/day.

While the recommended dietary intake of vitamin K is 90-120 mcg per day, the
optimal dose and form of vitamin K supplementation to achieve a protective
effect on bone loss and fracture reduction is not known. The majority of studies
used menaquinone-4 at doses approximately 400-fold higher than dietary
recommendations for vitamin K1. An additional issue is that these studies have
been conducted almost exclusively in Japanese postmenopausal women. This
population group may have unique dietary, environmental, and/or genetic factors,
so it is not clear whether the findings from these studies can be generalized to
other populations. In contrast to the 7 positive Japanese studies, a
double-blind trial in 381 postmenoapusal women received either phylloquinone 1
mg/day, MK4 45 mg/day or placebo for 12 months.42 No effect of phylloquinone or
MK4 on the bone density of the lumbar spine or proximal femur was observed.

Two long-term trials have previously been done evaluating the effect of vitamin
K1 supplementation on bone loss. In one study using 1 mg per day of vitamin K1
plus calcium and vitamin D for 3 years in postmenopausal women ages 50-60
years,43 bone loss was reduced at the femoral neck but there was no beneficial
effect on spine bone density. In a second study,44 200 mcg per day of vitamin K1
plus calcium and vitamin D given for two years to non-osteoporotic women aged 60
years or older resulted in a modest increase in bone mineral density of the
radius, but not the femoral neck.

Menaquinone-7 (a form of vitamin K2), which is derived from natto (fermented
soybeans) has been found in animal studies to be more potent and more
bioavailable, and to have a longer half-life, than menaquinone-4. In a study of
Japanese postmenopausal women, a significant inverse association was found
between natto consumption and the incidence of hip fractures.45

Conclusion

The most effective approach to osteoporosis is prevention. The risk of
developing osteoporosis may be reduced by optimizing peak bone mass in the
younger years and by minimizing subsequent bone loss in elderly women. In order
to maximize peak bone mass (even in the context of hereditary and other
non-modifiable risk factors), lifestyle habits, proper nutrition with a whole
foods diet, moderate exercise, and avoiding tobacco and excessive alcohol
consumption should begin during childhood and adolescence and continue
throughout life. The physician is encouraged to maintain a key interest in
dietary habits that promote optimal bone health, and include nutritional
supplementation that may favorably alter patients' risk and provide optimal bone
strength, bone architecture, and bone density with reduced risk for fractures
later in life.

References

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and supplementation with cholecalciferol for prevention of fractures in primary
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fracture risk in men and women: a meta-analysis of prospective cohort studies
and randomized controlled trials. Am J Clin Nutr 2007;86:1780-1790.
3Shea B, Wells G, Cranney A, et al. Meta-analyses of therapies for
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the prevention of postmenopausal osteoporosis. Endocr Rev 2002; 23:552-559.
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vertebral bone loss in perimenopausal women: a controlled trial in 248 women
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9Bischoff-Ferrari H, Willett W, Wong J, et al. Fracture prevention with vitamin
D supplementation: a meta-analysis of randomized controlled trials. JAMA
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10Dawson-Hughes B, Dallal G, Krall E, et al. A controlled trial of the effect of
calcium supplementation on bone density in postmenopausal women. N Engl J Med
1990;23:878-883.
11Bischoff H, Stahelin H, Dick W, et al. Effects of vitamin D and calcium
supplementation on falls: a randomized controlled trial. J Bone Miner Res
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12Pfeifer M, Begerow B, Minne H, et al. Effects of a short-term vitamin D and
calcium supplementation on body sway and secondary hyperparathyroidism in
elderly women. J Bone Miner Res 2000;15:1113-1118.
13Bischoff-Ferrari H, Dawson-Hughes B, Willett W, et al. Effect of vitamin D on
falls: a meta-analysis. JAMA 2004;291:1999-2006.
14Cohen L, Kitzes R. Infrared spectroscopy and magnesium content of bone mineral
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15Stendig-Lindberg G, Tepper R, Leichter I. Trabecular bone density in a two
year controlled trial of peroral magnesium in osteoporosis. Magnes Res
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16Mounier P, Roux R, Seaman E, et al. The effects of strontium ranelate on the
risk of vertebral fracture in women with postmenopausal osteoporosis. N Engl J
Med. 2004 Jan 29;350:459-468.
17Meunier, P, Slosman, D, Delmas, P, et al. Strontium Ranelate: Dose-Dependent
Effects in Established Postmenopausal Vertebral Osteoporosis--A 2-Year
Randomized Placebo Controlled Trial. J Clin Endocrinol Metab
2002;87:2060-2066.((Note: Only the first word of the title should be
capitalized.))
18Atik OS. Zinc and senile osteoporosis. J Am Geriatr Soc 1983;31:790-791.
19Follis RH Jr, Bush JA, Cartwright GE, Wintrobe MM. Studies on copper
metabolism XVIII. Skeletal changes associated with copper deficiency in swine.
Bull Johns Hopkins Hosp 1955;97:405-409.
20Smith R, Smith J, Fields M, Reiser S.. Mechanical properties of bone from
copper deficient rats fed starch or fructose. Fed Proc 1985;44:541.
21Eaton-Evans J, McIlrath EM, Jackson WE, et al. Copper supplementation and the
maintenance of bone mineral density in middle-aged women. J Trace Elem Exp Med
1996;9:87-94.
22Leach R, Muenster A, Weign E. Studies on the role of manganese in bone
formation. II. Effect upon chondroitin sulfate synthesis in chick epiphyseal
cartilage. Arch Biochem Biophys 1969;133:22-28.
23Strause L, Saltman P, Smith KT, et al. Spinal bone loss in postmenopausal
women supplemented with calcium and trace minerals. J Nutr 1994;124:1060-1064.
24Nielsen FH. Boron—an overlooked element of potential nutritional importance.
Nutr Today 1988;Jan/Feb:4-7.
25Anonymous. Silicon and bone formatin. Nutr Rev 1980; 38:194-195.
26Hott M, de Pollak C, Modrowski D, Marie P. Short-term effects of organic
silicon on trabecular bone in
mature ovariectomized rats. Calcif Tissue Int 1993, 53:174-179.
27Van Neurs J, Dhonukshe-Rutten R, Pluijm S, et al. Homocysteine levels and the
risk of osteoporotic fractures. N Engl J Med 2004;350:2042-2090.
28Brattstrom L, Hultbnerg B, Mardebo J. Folic acid responsive postmenopausal
homocysteinemia. Metabolism 1985;34:1073-1077
29Sato Y, Honda Y, Iwamoto J, et al. Effect of folate and mecobalamin on hip
fractures in patients with stroke: a randomized controlled trial. JAMA
2005;293:1082-1088.
30Barber G, Spaeth G. Pyridoxine therapy in homocystinuria. Lancet 1967;1:337.
31Dodds RA, Catterall A, Bitensky L, Chayen J. Abnormalities in fracture healing
induced by vitamin B6 deficiency in rats. Bone. 1986;7:489-495.
32Silberberg R, Levy BM. Skeletal growth in pyridoxine deficient mice. Proc Soc
Exp Biol Med.1948;67:259-263.
33Benke PJ, Fleshood HL, Pitot HC. Osteoporotic bone disease in the
pyridoxine-deficient rat. Biochem Med. 1972;6:526-535.
34Azuma J, Kishi T, Williams RH, Folkers K. Apparent deficiency of vitamin B6 in
typical individuals who commonly serve as normal controls. Res Commun Chem
Pathol Pharmacol 1976;14:343-348.
35Hyams DE, Ross EJ. Scurvy, megaloblastic anemia and osteoporosis. Br J Clin
Pract 1963;17:332-340.
36Ducy, P, Desbois C, Boyce B, et al. Increased bone formation in
osteocalcin-deficient mice. Nature. 1996;382(6590):448-452.
37Booth SL, Tucker KL, Chen H, et al. Dietary vitamin K intakes are associated
with hip fracture but not with bone mineral density in elderly men and women. Am
J Clin Nutr 2000;71:1201-1208.
38Feskanich D, Weber P, Willett WC, et al. Vitamin K intake and hip fractures in
women: a prospective study. Am J Clin Nutr 1999;69:74-79.
39Booth S, Dallal G, Shea K, et al. Effect of vitamin K supplementation on bone
loss in elderly men and women. J Clin Endocrinol Metab 2008;93:1217-1223.
40Cheung A, Tile L, Lee Y, et al. Vitamin K supplementation in postmenopausal
women with osteopenia (ECKO Trial): A randomized controlled trial. PLoS Med.
2008 Oct 14;5(10):e196.
41Cockayne S, Adamson, J, Lanham-New S, et al. Vitamin K and prevention of
fractures. Systematic review and meta-analysis of randomized controlled trials.
Arch Intern Med 2006;166:1256-1261.
42Binkley N, Harke J, Krueger D, et al. Vitamin K treatment reduces
undercarboxylated osteocalcin but does not alter bone turnover, density or
geometry in healthy postmenopausal, North American women. J Bone and Mineral
Research 2009;24(6):983-991.
43Braam L, Knapen M, Geusens P, et al. Vitamin K1 supplementation retards bone
loss in postmenopa-usal women between 50 and 60 years of age. Calcif Tissue Int
2003;73:21-26.
44Bolton-Smith C, McMurdo M, Paterson C, et al. Two-year randomized controlled
trial of vitamin K1(phylloquinone) and vitamin D3 plus calcium on the bone
health of older women. J Bone Miner Res 2007;22:509-519.
45Kaneki M, Hedges S, Hosoi T, et al. Japanese fermented soybean food as the
major determinant of the large geographic difference in circulating levels of
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2001;17:315-321.

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Recipes: Crescent Moon Cookies

 

Good Morning!

Recipes: Crescent Moon Cookies

These cookied can be made to celebrate the Crescent moon!
Yet another one of my mother's specialties, these delicious cookies are always a favorite around Christmas time. It is impossible to stop at just one of these absolutely yummy almond crescent cookies. Infused with vanilla and lightly dusted with sugar, these beautiful cookies are crunchy on the outside and soft, buttery and crumbly on the inside.

Ingredients:

1 cup butter, at room temperature
2/3 cups granulated sugar
2 tsp pure vanilla extract
2 1/2 cups all-purpose flour, sifted
1 cup ground almonds (almond meal)
1/4 cup confectioner's sugar for dusting

Directions:

1.Place the butter and the sugar together in a large mixing bowl and use a electric hand beater to mix until light and fluffy for about 5 minutes. Add vanilla extract and mix well.

2.Add the flour and almonds. Mix thoroughly.

3.Line baking sheet with baking paper. Preheat the oven to 350F

4.The dough will be slightly crumbly. Take generous tablespoons of the dough and roll into a small ball, about 1" in diameter. Shape into a crescent shape. Place onto baking sheet about 1" apart. Bake for 15-20 minutes or until a light golden brown. Remove from oven and dust with confectioner's sugar. Allow to cool on baking sheet for 5 minutes then transfer to a wire rack to cool. Re-dust with sugar.

5.Repeat with remaining dough.

6.Store in an airtight container.

Make about 24 cookies

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How to Make Cultured Veggies at Home to Boost Your Immune System

Your digestive tract is probably the most underappreciated system of your body, often ignored until its screams of discontent become loud enough to grab your attention.

By the time your gut reaches this degree of disgruntlement, the problems have usually been developing for months — or years — and are challenging to resolve.

Instead of waiting for obvious signs of a problem, why not perform some regular “gut maintenance” that will lessen your chances of developing a problem in the first place?

Your gut is much more than a food processing tube — it houses about 85 percent of your immune system. This is in large part due to the 100 trillion bacteria that live there, both good and bad that can stimulate secretory IgA to nourish your immune response.

When your GI tract is not working well, a wide range of health problems can appear, including allergies and autoimmune diseases. If you suffer from any major illness, you simply will NOT be able to fully recuperate without healing and sealing your gut. Balancing the menagerie of microorganisms that occupy your GI tract is a key part of maintaining your immune health, which will be the focus of this article.

Your stomach is where digestion really gets rolling, with the introduction of more enzymes and a whole lot of acid. Fortunately, your stomach is uniquely designed for this process, as it is SO acidic. Its lining must actually regenerate at a feverish pace — just to keep up with the continuous digestion of itself! You require a brand new stomach lining every few days.
Your Stomach Actually Protects You from Infections

A recent article in Scientific American1 explores an alternate explanation about how your stomach works. The “sieve hypothesis” suggests your stomach may operate as a sieve or filter, preventing some of the more harmful microbes from passing through to your small intestine. Evidence for this is not new. It comes from a 1948 study by Dr. Orla-Jensen, a retired professor from the Royal Danish Technical College — a study that has essentially been “lost” in the literature for more than 60 years.

The professor argued that your stomach uses acid to kill pathogenic disease-causing bacteria, fungi, viruses, worms and protozoa, while allowing the more beneficial microbes (which are acid-tolerant) to pass through. If your stomach is unsuccessful at killing these pathogens, then they can dominate your intestines, damaging and eroding your intestinal walls and causing illness.

Your stomach generally becomes less acidic as you age, particularly after age 70. In his study, Orla-Jensen compared the gut bacteria of young people with that of healthy seniors, as well as with seniors suffering from dementia. He found that as people age, they have a greater proportion of pathogenic microbes to beneficial microbes in their intestinal tracts. This was particularly pronounced in seniors with dementia... which begs the question about whether dementia could actually be caused by an “intestinal infection.”

A study done at UC Davis found that E. coli and salmonella bacteria in mice produce fiber-like structures very similar to the inflammatory brain plaques seen in people with Alzheimer’s disease2. Your brain is shaped by bacteria in your digestive tract. Bacteria in your gut actually control how your brain cells express specific genes.3 Other studies report that disturbed gut flora in seniors contributes to accelerated aging, frailty and premature death.

More research is needed in order to understand the exact relationship between dysbiosis and dementia. But at the very least, these studies underscore the importance of maintaining high levels of beneficial bacteria in your intestinal tract. In fact, this bacterial community may be in charge of your entire metabolism.
Unhappy Gut Bacteria May Make You Fat

Inflammation from bacterial endotoxins may be a factor helping to drive the obesity epidemic.4 Junk food causes nasty microbes to bloom and friendly bugs to decline, just as sugar and refined carbohydrates feed the bacteria in your mouth that are responsible for tooth decay. Sugar and processed foods make your “friendly” microbe community unfriendly — even downright hostile. Humans today have lost the microbial diversity that once kept us healthy.

When dysbiosis occurs, bacteria release noxious byproducts called endotoxins. Endotoxins increase the permeability of your gut wall (“leaky gut syndrome”) and make their way into your bloodstream, triggering system wide inflammation. It’s been shown that the hypothalamus, which houses the appetite control center of your brain, is often inflamed and damaged in obese individuals. When inflammation affects your brain, and especially your hypothalamus, your entire metabolism changes.

So, here’s how it goes...

When you consume junk foods, certain bacteria flourish and produce endotoxins, which your immune system detects and, interpreting these endotoxins as an attack, responds with inflammation. Your body changes its metabolism to redirect energy for “battle.” The result is overproduction of insulin, increased fat storage, dampening of your appetite control signals, and eventually obesity. The best way to reverse this inflammation and restore a healthy metabolism is by eliminating excess sugar and processed food, and adding more friendly, beneficial bacteria from naturally fermented foods.
Cultured Vegetables Are the Ultimate Superfood

One of the leading experts in the optimization of intestinal flora is Dr. Natasha Campbell-McBride, who developed the GAPS nutritional protocol (Gut and Psychology Syndrome/Gut and Physiology Syndrome). For decades, Dr. McBride has successfully treated adults and children with severe illnesses, including autism, epilepsy, mood disorders, arthritis, multiple sclerosis, celiac disease and many more, with her GAPS protocol.

A key component of the GAPS program is the daily consumption of fermented foods. Fermented foods are potent chelators (detoxifiers) and contain much higher levels of probiotics than probiotic supplements, making them ideal for optimizing your gut flora. In addition to helping break down and eliminate heavy metals and other toxins from your body, beneficial gut bacteria perform a number of surprising functions, including:
Mineral absorption, and producing nutrients such as B vitamins and vitamin K2 (vitamin K2 and vitamin D are necessary for integrating calcium into your bones and keeping it out of your arteries, thereby reducing your risk for coronary artery disease and stroke5)
Preventing obesity and diabetes, and regulating dietary fat absorption
Lowering your risk for cancer
Improving your mood and mental health
Preventing acne
Introducing Cultured Vegetables into Your Diet — The Right Way
Now that you understand the importance of optimizing your GI flora, let’s take a look at just how easy it is to accomplish this task by making fermented vegetables at home, in your own kitchen. If you aren’t accustomed to these foods, you may have to work them into your diet gradually. Many folks really enjoy the taste of fermented vegetables, which really have a pleasantly salty-tart flavor.

According to nutritional consultant Caroline Barringer, just one quarter to one half cup of fermented veggies, eaten with one to three meals per day, can have a dramatically beneficial impact on your health.

If you’ve never eaten fermented foods, too large a portion may provoke a healing crisis, which occurs when the probiotics kill off pathogens in your gut. When these pathogens die, they release potent toxins. If you are new to fermented foods, you should introduce them gradually, beginning with as little as one teaspoon of sauerkraut with a meal. Observe your reactions for a couple of days before proceeding with another small portion, and increase your dose gradually, as tolerated.

Realize that many food preferences develop very early in life, so the sooner you can introduce fermented vegetables to your child, the better. Traces of the flavors of the foods mothers eat are perceptible in their breast milk and amniotic fluid. Babies whose mothers eat things like garlic or broccoli while pregnant tend to be more likely to enjoy these foods later in life.
Making Cultured Veggies at Home: Equipment Checklist

Culturing your own vegetables is not difficult, but as with anything, having the right tools makes the job much easier and more fun. I have spent the last six months streamlining the process and refining my basic recipe. One of the key ingredients though is the starter culture. We are in the middle of a very extensive testing process to provide a culture that will give you large amounts of vitamin K2 in your fermented vegetables. We hope to have that available later this year if all goes well. In the meantime, you can use the following kitchen tools to make your own fermented vegetables:
Food Processor: You’ll be cutting up large quantities of raw vegetables, which is very labor intensive without a food processor. Make sure yours has a shredding disc, as a typical S-blade will result in too fine a chop, which makes for a pulpier, mushier end product.
Juicer: My own experimentation has resulted in selecting celery juice as the basic brine for my cultured veggies, making a juicer necessary.
Good Knives: Make sure you have a set of good quality, sharp knives for prepping your vegetables.
Cutting Board: A large, sturdy cutting board is a must.
Very Large Bowl: This bowl should be large enough to hold the entire batch of shredded veggies, so a large capacity stainless bowl is a necessity.
Canning Jars: Basic wide-mouthed 32-ounce Mason jars are all that is necessary for both fermenting and storing the vegetables. These are inexpensive and easy to find at your local hardware store, grocery, or online. Make sure they are wide-mouthed, as you’ll need to get your hand or a tool down into the jar for tightly packing the veggies.
Krautpounder: This solid wood tool that looks like a small baseball bat is very handy for tightly packing the shredded veggies into your jars and eliminating air pockets.
Making Cultured Veggies at Home in Six Easy Steps

The following are the basic steps to making wonderful cultured vegetables at home. For additional information, refer to our previous article on this topic.
Vegetable and Herb Selection: The first step is gathering up your veggies. Make sure they are all organic. Cabbage (red or green) should be the “backbone” of your blend, comprising about 80 percent (I use green). Choose dense, tightly packed heads. Five or six medium-sized cabbages will yield 10 to 14 quart jars of fermented vegetables. Remember to reserve some cabbage leaves for the jar tops (see Step 3).

Add in hard root vegetables of your liking, such as carrots, golden beets, radishes and turnips. Peel your veggies as the skins can impart a bitter flavor. I also enjoy adding red bell pepper, Granny Smith apples, and even a hot pepper, like a habanero (make sure you wear gloves!). One pepper for the entire batch is plenty.

Aromatics can be added in small quantities — a little goes a long way, as fermenting concentrates the pungent flavors. Tasty additions include peeled garlic, peeled ginger, and herbs such as basil, sage, rosemary, thyme, or oregano. Onions tend to overpower the mix, no matter how little are used, so I avoid them.

Finally, you can add sea vegetables or seaweed to increase the mineral, vitamin, and fiber content. You can add pieces of whole dulse, or use flakes. Wakame and sea palm do not have any kind of fishy flavor but need to be presoaked and diced into the desired size. Arame and hijaki DO have a fishy flavor.
Culture and Brine: For your brine, I recommend using a starter culture dissolved in celery juice. One quart of celery juice is adequate for 10 to 14 quarts of fermented veggies. While you can do wild fermentation (allowing whatever is naturally on the vegetable to take hold), this method is more time consuming, and the end product is less certain. Inoculating the food with a starter culture speeds up the fermentation process. I currently recommend using two of our Complete Probiotics as the starter culture until we get our refined version which will make more vitamin K2.
High Vitamin K2 Starter Culture As I said above, we are in the middle of a very extensive testing process to provide a culture that will give you large amounts of vitamin K2 in your fermented vegetables and we hope to have that available later this year if all goes well. In the meantime i recommend using two of our Complete Probiotic Capsules for every quart of fermented vegetables as that is very close to what our final culture will be.
Packing the Jars: Once you have your shredded veggies and brine mixture combined in your large bowl, tightly pack the mixture into each Mason jar, and compress using a masher to remove any air pockets. Top with a cabbage leaf, tucking it down the sides. Make sure the veggies are completely covered with brine and that the brine is all the way to the top of the jar, to eliminate trapped air. Put the lids on the jars loosely, as they will expand due to the gases produced in fermentation.
Fermentation: Allow the jars to sit in a relatively warm place for several days, ideally around 72 degrees Fahrenheit. During the summer, veggies are typically done in three or four days. In the winter, they may need seven days. The only way to tell when they’re done is to open up a jar and have a taste. Once you're happy with the flavor and consistency, move the jars into your refrigerator.
Storage: Refrigerating your vegetables drastically slows down the fermentation. They will keep for many months this way, continuing to mature very slowly over time.
Enjoy! Always use a clean spoon to take out what you’re eating. Never eat out of the jar, as you will contaminate the entire batch with bacteria from your mouth. Make sure the remaining veggies are covered with the brine solution before replacing the lid.