Vitamins to Breast Cancer

This popular and vital topic is used as a Real Life example to show how difficult if is for Scientists to analyze the many factors that have to be considered when evaluating possible vitamin health connections.

Scientists have mountains of data to study to find connections. The interpretation of current research presents many challenges for the development of new health theories, especially when study results differ from existing mainstream health protocols.

First one lists discovered facts and associations gained from past research to see how they might fit together as puzzle pieces with new study results. Breast cancer connections are listed below as an example. These are just in most cases associations and not cause and effect facts. Work with your Medical team if you have this condition.

1. Breast cancer rates are slightly higher after menopause in women with increased bone density. ref ref
2. Calcium and vitamin D may increase bone density.
3. Weight-bearing exercise increases bone density and strength.
4. Overall, Exercise decreases breast cancer risk. ref  ref
5. Exercise increases available oxygen for cells and tissues.
6. Higher Magnesium levels, but not calcium, associated with better survival from breast cancer. ref
7. Higher estrogen levels maintain greater bone density
8. Higher estrogen levels are associated with greater breast cancer risk (estrogen positive cancers) ref
9. Since estrogen is built in fat tissue, this might be one way obesity is related to greater breast cancer risk, but blood sugar may also be a factor.
10. Drugs to slow bone turnover and bone growth reduce breast cancer rates, i.e. bisphosphonates like Fosamaxtm
11. Bone Hormone Osteocalcin levels are increased with higher bone turnover.
12. Osteocalcin helps regulate blood sugar and insulin levels (NEW).  ref
13. Osteocalcin is built by bone building cells under guidance of vitamin D.  ref  
14. In test tube studies, Vitamin D exhibits a biphasic role on osteocalcin production with opposite direction responses on vascular calcification at different vitamin D levels.*** ref
15. Osteocalcin exists in two forms, uncarboxylated (ucOC) and carboxylated (cOC).
16. Osteocalcin is built under vitamin D direction as uncarboxylated, after carboxylation by vitamin K2, Osteocalcin helps bind calcium into bones. article   ref
17. Breast cancer patients with higher levels of adiponectin, produced under direction of osteocalcin in fat cells, survived longer. ref  (Raspberry Ketone studies on animals show increased expression of adiponectin ref , still needs human verification)
18. The active hormone form of vitamin D inhibits Breast cancer cells from producing HAS-2, an enzyme that builds hyaluronic acid which cancer cells hijack (ref)and use to trigger inflammation and the building of new blood vessels to feed and grow tumors bigger, CD44 attaches to HA to accomplish this action. ref
19. Breast cancer patients often exhibit higher blood sugar levels and lower osteocalcin levels if bones are not involved, where in that case, osteocalcin levels are increased over normal.  ref  ref
20. Insulin and /or insulin growth factor (IGF-1) levels are elevated in breast cancers. ref  ref  ref
21. IGF-1 is increased in cows given the growth hormone rBGH, and thus in their milk too.
22. Cancer cells have numerous insulin receptors which feed off higher insulin levels to protect the cancer cells from anticancer drugs. Some anticancer drugs increase insulin resistance that further reduces their therapeutic effect. ref 
23. It is the fructose in High fructose corn syrup and table sugar that increases BC development and spreading to lungs ref ref
24. Multiple Vitamin use increases DNA repair capacity which decreases breast cancer risk. ref
25. While Multiple Vitamin use increased cancer risk in this study. ref Need to check for differences between locations for other factors to solve this situation.
26. This study showed no real differences between multiple vitamin use and BC, but some differences in a few subsets. ref  Maybe a factor between 23 and 24 above.
27. Women with higher blood levels of carotenoid family have reduced risk for BC. ref  
28. Small studies so far show CoQ10 might restore the death sequence to cancer cells. ref ref
29. RANKL, a ligand necessary to regulate normal and balanced bone rebuilding, is found at increased levels in breast cancer cells. article  ref
30. Chemotherapy drugs and radiation can lead to greater p53 damaged genes. Healthy p53 is activated to stop cancer cell growth, but when mutated does not provide this action. ref  Over 50 percent of cancers including breast cancer exhibit mutations in p53. ref There are natural food elements that prevent p53 damage and restore p53 functions, such as SGS in broccoli. (In other cancers, p53 can be over expressed which also is counter to healthy cells.)
31. The enzyme Aromatase converts androgen to estrogen. It is found at increased levels in breast cancer than in normal breast tissues. Grape seed extract (GSE) contains high levels of procyanidin dimers that are known potent inhibitors of aromatase.
32. A form of vitamin E, alpha tocopherol succinate, exhibits potential to destroy cancer cells and leave normal cells untouched. In fact, it protects the normal cells. ref
33. A form of synthetic vitamin E exhibits far superior action to destroy cancer cells than the natural form as alpha tocopherol. A vitamin E family member, Gamma tocopherol, was also effective and in some cases, even more effective than the synthetic alpha E analogue form. ref 
34. Cancer cells are unable to break apart the synthetic vitamin E analogue to neutralize it's cancer killing potential. Nutritional vitamin E as alpha tocopherol does not exhibit this cancer killing effect, while Gamma tocopherol does in it's natural form. Another reason to use all the family members of vitiamin E instead of just the Government mandated only alpha tocopherol form. A 70 year old vitamin mistake.
35. Women with a BRAC1 or BRAC2 mutation plus higher levels of folates, exhibit a higher risk of BC. ref check out date of this study. Suggests need for more research. Look at this older study. ref 
36. Timing and amounts of dietary folates and supplemental folic acid reveal a U shaped curve for effects. Adverse at under 150mcg /day or over 400mcg/day. Healthy protection in-between, with more prevention before disease and acceleration of disease once established. ref 
37. Over the last 3 years, an intensive research has developed that shows significant BC growth reduction using vitamin A factors all-trans retinoic acid and 9-cis retinoic acid. The results were in the right direction, but not at a desired level. So synthetic derivatives from these two natural vitamin A forms were developed that are reaching 60 to 80% reductions in marker proteins associated with BC spreading ability. ref ref ref 
38. Over the last decade, research has found an association between the gut microbiotia and the risk of breast cancer. ref Harmful bacteria are also foound in the tissues of people with breast cancer versus those without. In the future, brest cancer treatments may include a reinduction of a favorable bacteria mix.
39. Healthy mix of bacteria in the colon also is responsible for the elimination of excess estrogens while unhealthy bacteria strains reasorb estrogens back into the body.                        

***Here is part of conclusion from this referenced study..."vitamin D exerts a biphasic 'dose response' curve on vascular calcification with deleterious consequences not only of vitamin D excess but also of vitamin D deficiency"

The complexity of these facts tends to cloud some issues. Finding a common thread out of these facts, observations, and associations is paramount to developing an effective protocol for treatment and of more importance, prevention. Check this review out, Copied here to prevent loss of link:

"Breast Cancer Res Treat. 2012 Jul 25. [Epub ahead of print] Dietary calcium intake, vitamin D levels, and breast cancer risk: a dose-response analysis of observational studies.

Hong Z, Tian C, Zhang X. Source Kunshan Municipal Center for Disease Control and Prevention, Kunshan, 215300, Jiangsu, People's Republic of China.

Abstract Results from the recent meta-analysis suggested a favorable effect of dietary calcium and vitamin D levels on breast cancer risk. However, the relationship of dietary calcium and vitamin D levels with breast cancer risk is unclear. Thus, the dose-response relationship was assessed by restricted cubic spline model and multivariate random-effect meta-regression. Results suggested that women might suffer from the lowest risk of breast cancer with dietary calcium intake of about habitually around 600 mg/day, dietary vitamin D intake of about 400 IU/day, and serum vitamin D levels of about 30 ng/ml. PMID: 22872547" 

You probably are not amazed that these levels are within the recommendations of the new Vitamin Crieteria.

Then along comes another study showing that the ratio of uncarboxyated osteocalcin to carboxylated has greater influence over the osteocalcin and adiponectin relationship to insulin resistance, blood sugar levels, and energy metabolism than previously thought.  ref

There exists a strong feedback loop between many if not all of these factors to control the energy metabolism and bone control mechanisms with a resulting influence over breast cancer development and promotion. A greater understanding for the systems operating in breast cancers are now known. Vitamins D3 and K2 represent vital links in this protocol. Vitamin D to synthesize osteocalcin production and vitamin K2 to regulate the balance between uncarboxylated and carboxylated osteocalcin since both probably play important roles in the energy metabolic and bone health pathways; insulin secretion and resistance, blood sugar level control of glucose, adiponectin balance, estrogen support, bone turnover with balanced building and tearing down rates. Of course exercise, weight maintenance, and dietary patterns all have significant roles to play as well.

Questions that arise from these facts:

• Why does higher bone density equate with more breast cancers?    There are at least 4 things that can lead to increased bone density:  

1. Genetics for body and bone size and hormone balance (higher estrogen levels strongly implicated in breast cancer rates)   
2. Weight-bearing exercise (Probably not a factor since athletes have lower overall cancer rates, Could be related to oxygenation of tissues preventing cancer development, or increased efficiency of anti-oxidant load balance)   
3. Being overweight stresses bone to become stronger (especially gaining weight as an adult which could be hormone balance related, especially thyroid),(see Note 1 below)    
4. Consuming proper amounts of calcium from foods or supplements and/ or vitamin D as well as fruits and vegetables (some reduced cancers from calcium and D intake, but generally benefits observed with greater intakes of fruits and vegetables).

SIDEBAR: While the extra weight in obese women puts stress on bones similar to exercise and many have higher bone mineral density, another factor also puts them at risk. When the body overall is obese, extra fat enters bones and develops bone marrow fat. This increases the risk for osteoporosis. ref

TAKE AWAY

This discussion is more for general interest to show complexity of theory generation rather than actual use of facts presented. But, the threads presented here might stir awareness of the relatedness of different processes to cancer characteristics. See this article for further discussion. Perhaps, the most important take away is that many nutrients have an optimal window of intake amounts that presents the greatest benefits.

In number 34 above, the retinols are from vitamin A or Beta Carotene sources. Beta carotene comes in at least 4 different forms in nature, all-trans RA, 9-cis RA, 11-cis RA, and 13-cis RA. Synthetic beta carotene in the vast majority of multiple vitamins is only the syntheic all-trans RA form. Eat your vegetables to get all forms, or take a multiple vitamin with algae source beta carotene. Most pre-formed vitamin A in multiples is also synthetic.

Both too low and too high can exhibit adverse reactions. Vitamin D comes to mind here. The latest tendencies are to overcome vitamin D deficiencies by pushing vitamin D levels too high. And look at body weight, higher is protective of bone strength but begins to increase breast cancer risk. Where is the happy medium and balance point? Why is science not rapidly searching for this vital information?

OF INTEREST: A Vitamin Study out of Sweden looking at multiple vitamin use on breast density found an association. Yes, there are certain vitamins that might increase growth of breast tissue or relate to greater breast tissue density. Genetics of course plays the largest part. Folic acid and vitamin C come to mind. Folic acid increases cell turnover rates and vitamin C directs collagen production. Collagen participates in breast tissue density by building connective tissues. While this topic is still exploding with studies and more research results will shortly be surfacing, see this article for more. 

Scientific Method Failures and Physiology Faults in Vitamin Applications

In order for Science to arrive at correct vitamin theories, it cannot operate under faulty or incomplete vitamin and health premises. When you understand the current flaws in vitamin concepts, everything else like results from controversial research fits together like nature intended. These are some major physiological flaws:  

• The Body has an Anti-Oxidant Load Balance Point    

The body operates by maintaining harmony and balance in all functions and processes. If more free radicals are generated, such as during exercise, natural body produced anti-oxidants are also generated, or made more efficient, or kept from being destroyed as quickly, to keep these two opposites in balance. When illness causing viruses attack the body, the immune system reacts by having White Blood cells generate free radicals that function to destroy viruses. As long as the anti-oxidant load is in balance, the viruses are destroyed in a timely manner. But if anti-oxidants are consumed at overload amounts, the WBC generated radicals could be destroyed before they have completed killing the attacking viruses and or bacteria.  ref

NOTE: Analyzing the anti-oxidant amounts in some wellness supplements, it becomes obvious that the formulators of these products lacked this basic knowledge of how the body protects itself and destroys cold viruses. Not only does the body use free radicals to attack and kill viruses, it also uses the free radical ROS to help destroy cancer cells. An ingredient in fruits and vegetables called apigenin generates ROS in cells to increase this destructive pathway. Apigenin belongs to the flavonoid group in fruits and vegetables which also includes myricetin, quercetin, kaempferol, and luteolin, etc. Very important cancer prevention >  ref

Certain supplements like selenium naturally increase the body's anti-oxidant load. If one is low in selenium and thus also potentially low in one of the important cellular anti-oxidants, glutathione peroxidase (GP) built from selenium, the increased supplemental selenium helps to balance. BUT, if the body is already supplied with the proper amount of selenium, adding extra pushes the anti-oxidant GP production out of balance. This can have an adverse effect on body health and can exhibit a negative influence on the results of vitamin research.

In the SELECT study testing vitamin E and selenium on Prostate Cancer prevention, the opposite of the expected result was observed. Vitamin E group had slightly more prostate cancer while the selenium group exhibited a slightly higher diabetes rate. Yes, both of these observations are related to the anti-oxidant / redox balance. ref ref

Extra selenium must have increased GP levels in some of the test group up to an amount where the anti-oxidant load exceeded the balance point for control of certain free radicals. The body uses these free radicals to switch on glucose insulin uptake by cells. The increased anti-oxidant load simply destroyed the needed free radicals before they could activate the switch for glucose insulin uptake. 

The vitamin E group was only given the alpha tocopherol part of vitamin E, which is very effective against oxygen radicals that attack the prostate. But nitrous radicals also attack prostate tissues. These need another family member of vitamin E to destroy them, gamma tocopherol. In fact, there may be more nitrous than oxygen radicals generated in the prostate. Taking just alpha tocopherol actually hinders the absorption of gamma from food and lowers the amount of this nitrous radical destroying form in the blood. This leaves more than half the prostate tissue unprotected. Studies after the SELECT research ended early have found positive results using both vitamin E forms together.

• Nutritional Science operates as if all vitamin forms are interchangeable  

Natural with synthetic? Some synthetic versions of natural vitamins are not identical and do not have the same function or process activity levels, especially the fat soluble vitamins A, D, E & K. If a synthetic version is used in a study, the protocol of the Scientific Method dictates that the results must specify this information in the result statement. But far too often, the Scientific Community generalizes results to imply both the natural and synthetic forms because they do not officially recognize any vitamin form differences or family symbiotic relationships. Science has now proven without question that these differences exist. Some Scientists and Nutritionists must still be operating under the past faulty assumptions. 

OF INTEREST: It is puzzling to note that when synthetic vitamin E was first synthesized and tested against the natural, scientists observed a significant difference. They had to use about 40% more synthetic material than the amount of natural vitamin E form to match the activity being measured. So 1.33 mg of synthetic vitamin E became equal to 1 mg. of natural. Dogs were used in those tests. Recently in human studies, Scientists measuring vitamin E tissue levels rather than just blood levels have discovered that the real equal amount for synthetic E is about double the amount of the natural. Does this mean the 1941 tests were not really correct and a faulty theory has served as the basis for nutritional applications for over 70 years? ...Yes, it appears so!

Developing Cancer Theories

Over the years, many alternative theories about cancer treatments have existed and some presented in their short runs some intriguing concepts that may yet prove part of a successful cancer protocol. Here are two examples: Dr Asai's development of GE-132 and the other is the use of an apricot kernel extract naturally containing the toxic element, cyanide. The theory for apricot kernels was that only cancer cells contained the enzyme necessary to release the cyanide from it's protective compound form. This would then allow the free cyanide to only kill the cancer cell. It might not really be that specific at only targeting cancer cells as this reference reveals. This aspect that cancer cells produce unique elements formed only in cancer cells and not by normal cells is an avenue Scientists are exploiting to destroy the cancer. Indeed this concept today is at the heart of the direction science is focusing in it's attempt to find a cure, or as the more realistic goal, turning cancer into a disease one could live with that would not spread and kill.

The GE-32 compound uses another cancer theory that says increasing oxygen into the system is not conducive to cancer cell survival (exercise effect). Plus, the Germaniun carrier of this increased oxygen might also play a similar role to cyanide in the apricot kernel reaction. ref  The FDA reviewed both of these theories and ruled the risk of adding toxic substances into the body did not justify any yet to be scientific method proven benefits.  ref

But, the critical aspects these two theories operated under is proving today to yield immense rewards to finding a workable and safe cancer treatment. Any moment now amazing cancer breakthroughs are expected. The just discovered IV vitamin C connection to inhibit HIF-1, an enzyme cancer cells produce to allow them to get enough energy, may be one of these valuable finds. ref  ref  A Turmeric element called curcumin shows natural anti-cancer properties by limiting NF-KB activity, similar to the action of aspirin. They both act to control inflammation.

Another vital link in the cancer arsenal includes the flavonoids from fruits, vegetables, herbs, and teas. The next reference is an easy read and very complete regarding the actions of flavonoids, especially apigenin, to prevent cancer cell growth, a process that includes upregulating DR5. ref ref 

Copied here is definition for what DR5 does to prevent loss of link. "Death receptor 5 (DR5), also known as TRAIL receptor 2 (TRAILR2) and tumor necrosis factor receptor superfamily member 10B (TNFRSF10B), is a cell surface receptor of the TNF-receptor superfamily that binds TRAIL and mediates apoptosis." This means it causes a process that allows cancer cells to die.

TELOMERASE  Another area under research includes the function of telomeres and their control of the lifespan of normal cells. Telomeres participate in a process that destroys normal cells after a regular lifetime, but cancer cells either have a dysfunctional telomere or use an enzyme that stops telomere control of cell lifespan which means they literally exist forever.  ref ref 

There is a fine line to balance this ability to play with the telomere enzyme since it also controls functions in every type of normal cell that must be respected.

Of interest: Another way to increase telomere length, or reduce speed of shortening, is to maintain adequate vitamin D levels. Copied here is a study showing this result on leukocytes. This could mean a slightly longer and possibly healthier life span but is still questionable on influence of cancer cells, but possibly through the control of inflammation.

"Am J Clin Nutr. 2007 Nov;86(5):1420-5.

Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women.

Richards JB, Valdes AM, Gardner JP, Paximadas D, Kimura M, Nessa A, Lu X, Surdulescu GL, Swaminathan R, Spector TD, Aviv A. Twin Research and Genetic Epidemiology, St Thomas' Hospital, King's College, London School of Medicine, London, United Kingdom. brent.richards@kcl.ac.uk

Abstract

BACKGROUND: Vitamin D is a potent inhibitor of the proinflammatory response and thereby diminishes turnover of leukocytes. Leukocyte telomere length (LTL) is a predictor of aging-related disease and decreases with each cell cycle and increased inflammation.

OBJECTIVE: The objective of the study was to examine whether vitamin D concentrations would attenuate the rate of telomere attrition in leukocytes, such that higher vitamin D concentrations would be associated with longer LTL.  DESIGN: Serum vitamin D concentrations were measured in 2160 women aged 18-79 y (mean age: 49.4) from a large population-based cohort of twins. LTL was measured by using the Southern blot method.

RESULTS: Age was negatively correlated with LTL (r = -0.40, P < 0.0001). Serum vitamin D concentrations were positively associated with LTL (r = 0.07, P = 0.0010), and this relation persisted after adjustment for age (r = 0.09, P < 0.0001) and other covariates (age, season of vitamin D measurement, menopausal status, use of hormone replacement therapy, and physical activity; P for trend across tertiles = 0.003). The difference in LTL between the highest and lowest tertiles of vitamin D was 107 base pairs (P = 0.0009), which is equivalent to 5.0 y of telomeric aging. This difference was further accentuated by increased concentrations of C-reactive protein, which is a measure of systemic inflammation.

CONCLUSION: Our findings suggest that higher vitamin D concentrations, which are easily modifiable through nutritional supplementation, are associated with longer LTL, which underscores the potentially beneficial effects of this hormone on aging and age-related diseases."

It is also interesting to note that multiple vitamin consumers have slightly longer telomere length than non-users. This would equate to possibly a little longer life.

How Trans Fats Damage Body

THE START OF TRANS-FATS

The rapid emergence of trans-fats from a bit player to a major force from margarines and Crisco in the American diet was the food industry's answer to the results of Ancel Keys' Seven Countries study on saturated fat increasing cholesterol leading to heart disease. Little did they know this was like jumping out of the frying pan and into the fire. Five years after this announcement, Keys discovered that he had made some factual errors in his first study and that saturated fat and cholesterol were not solely responsibly for heart disease. But by then, both modern medicine and the food industry had been so busy instilling this concept into the minds of Americans that the steamroller momentum could not be stopped, even by truth. What is this damage? ref

It is now known that Trans fats increase type 2 diabetes and heart disease, the very condition they were promoted to help prevent by the food industry. ref  Trans Fats lower the "good" HDL cholesterol and raise the "bad" LDL cholesterol. Here is how they do this. Plus, they are a marker for low bone density. To improve bone density, lower heart disease, and reduce type 2 diabetes, do not eat any of the foods listed here, or that have in their label box, the term - partially-hydrogenated oil. Plus the increase in dietary polyunsaturated vegetable oils replacing saturated fats promoted oxidation and inflammation leading to DNA damage and tumor development. ref  ref Whether or not a specific vegetable oil increases inflammation may depend upon the ratio of omega 3 to 6 in the oil and also already in the body. Trans-fats displace healthy fats in cell membranes but do not maintain the same membrane fluidity. ref  Membrane fluidity is a very important aspect of cell health by controlling what goes into and comes out of cells. ref A report found greater amounts of trans-fats in women with breast cancer. ref ref

ONE VITAL POINT ABOUT TRANS-FATS

In the process of making trans-fats by partial hydrogenation, vitamin K1 changes from it's natural form in green leafy vegetables as phylloquinone into 2,3,dihydophylloquinone. While this new form does some of vitamin K1 functions, it has a number of drawbacks for the complete range of K functions. First, less is absorbed, second, more is rapidly excreted, and third, it fails to impact and correct bone turnover markers. But perhaps the largest failing of dihydrophylloquinone is that it fails to convert into vitamin K2 as MK-4, a vital action for artery health, bone building, and also blood sugar control. ref ref ref To improve bone density, lower heart disease, and reduce type 2 diabetes, do not eat any of these dihydrophylloquinone containing foods listed here. 

Once in the body, trans-fats do not rapidly leave the body like other types of fats. Practically all of the phylloquinone in vegetable oils gets changed during hydrogenation into the dihydophylloquinone form. Since vegetable oils represent a major source for vitamin K1, the use of partially hydrogenated oils with mostly dihydrophylloquinone may be a significant aspect in the health of bones, cardiovascular disease, and blood sugar control. ref

WRAP UP

This one dietary change in the form of vitamin K from the rapid increase in foods containing trans-fats beginning in the 1950's could be responsible for a major share of related health conditions. This is also about the time that fast food restaurants became popular. Looking at heart disease, a disease of the 20th century, the rise and fall is almost parallel to the increased use of and the decreased availability lately of foods containing trans fatty acids. ref Could it really be this simple?

For more information, read this article. 

Nature, Infants, and Mother's Milk

NATURE, INFANTS, AND MOTHER'S MILK

If you were amazed over the infant cholesterol findings, this next topic blows the lid off any debate issues about the merits of breast-feeding versus bottle formula feeding. This can be summed up in one word: Oligosaccharides. or HMO for human milk oligosaccharides. Click on the term for easy reading about the critical value of infants getting these unique oligosaccharides only produced in human breast milk and their value to the health of the growing infant. ref ref ref ref ref

And this most interesting comparison between breast milk and bottle milk babies on developing Intestinal Microflora patterns. Another one here on bacteria types and delivery methods, etc.

Human Milk Enigma

Scientists analyzing human breast milk were dumbfounded to find this class of simple carbohydrates that the immature infant digestive tract was incapable of digesting. Why would Nature put oligosaccharides in breast milk if the infant could not digest them? 

After years of research, Scientists finally made a significant discovery. The oligosaccharides were not essentially for the infant at first, they were there to feed and help bacteria grow in the infant's developing intestinal tract. After lactobacillus in the small intestines and bifidobacteria in the colon used the oligsaccharides to grow more numerous, the bacteria would breakdown these carbohydrates into forms that the infant body could absorb and utilize as simple sugars. While many different bifidobacteria were able to digest a few oligosaccharides, there was only one strain of this bacteria that was capable of 100% digestion of human milk oligosaccharides and that bacteria strain is Bifidobacterium Longum subsp. Infantis. ref ref

Heading for Extinction in Breast Milk

In the past, B. Infantis was the dominate strain in the intestinal tract of every infant born. In the U.S. today, it is found in only about 1 in 10 infants. Plus, it is also absent in most Mothers. This reduction was a gradual process over many generations. The causes for this decline are numerous; use of antibiotics, C-section births ref, low fiber diets, processed foods, bottle formula feeding ref, sterilization and sanitation procedures, etc. 

Scientists are now conducting research to find out which if any of the numerous complaints present in infants might be related to the dissapearance of this vital bacteria strain; Gerd, colic, respiratory or digestive conditions, colds, allergies, ashma, skin rashes, obesity, even some cancers, etc. ref ref

Some of the oligosaccharides in human milk are unique to human mammary gland production and not found in cows milk. Plus, they cannot be made artificially yet, so no direct substitutes are available, but sources to mimic them are in the works to improve bottle formulas. ref  Enter prebioitcs, GOS, FOS, Inulin, and Lactoferrin. Most are available as Supplements. ref ref 

Supplements of B. Infantis appear to be mandatory at the moment. But, this will take perhaps a few generations to re-establish this necessary bacterium at levels necessary for widespread improvements in infant health. And perhaps some significant changes in current diets. Adults also benefit from this most valuable bacteria. Great references in this article, but caution, recommended products probably generate a kickback from a referral or affiliate program and may compromise choices offered. example

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