Another U.S. patent that depicts damage done by infant formula.  It is called
"Methods and preparations for the treatment and prophylaxis of metabolic
disturbances,"  with the inventor being Willem Serfontein of South Africa.  This
was filed in 1993 and is about a pharmaceutical or dietary supplement for
infants, particularly premature infants.
Valerie W. McClain, IBCLC

http://www.uspto.gov/patft/index.html
patent # 5631271

It therefore came as a great surprise, when the present applicant conducted
homocysteine measurements in the serum of new born and premature infants
(something which had never before been reported) and discovered an amazing
frequently of homocysteine abnormalities in such infants in addition to a number of
important additional findings.

It was found that average homocysteine levels in healthy infants (6-7
.mu.mole/l) are much lower than in adults (for whom up to 16.3 .mu.mole/l is normal).
However, surprisingly a relatively large proportion of infants were found to
have relatively elevated homocysteine levels. Based on experiments conducted
by the applicant on adults and various blood measurements carried out on the
infants, it was possible to reach conclusions as to causes and potential
consequences, and the present invention proposes appropriate countermeasures.

It was found that in ideal circumstances healthy infants, from healthy
mothers and wholly breast fed are protected naturally against elevated homocysteine
levels, a fact which indirectly confirms the danger residing in homocysteine.
In healthy new-born infants plasma levels of pyridoxal, vitamin B12 and folate
were found to be considerably higher than in adults. Applicant has
established that these high levels provide a natural protective mechanism against
accumulation of toxic homocysteine levels.

It was possible to correlate deficiencies in respect of one or more of the
aforegoing with elevated homocysteine levels in the respective infants and
detect connections with genetic factors, with pre-natal and post-natal maternal
nutritional status (the latter being relevant to breast fed infants). However,
most alarming of all was the discovery of the extent to which these elevated
homocysteine levels can be ascribed to bottle feeding with non-human milk and
milk formulae based on cow's milk. A careful assessment of certain differences
between human and non-human milk has revealed plausible causes for the
prevalence of homocysteineaemia amongst infants. In particular, cow's milk contains 4
times more methionine than mother's milk yet is lacking proportionally in
factors which would prevent or counteract the transformation of this excessive
amount of methionine into homocysteine.

Fraying and splitting of the vascular internal elastic membranes has been
observed as a clinical symptom of elevated homocysteine levels in adults. This
same symptom was described by Jaffe in 176 babies who had died of different
causes during their first 3 months of life. Sudden infant death syndrome has been
found to be particularly common amongst bottle-fed babies.

The vascular damage caused by homocysteine is well established. Research has
shown that this kind of damage is the primary cause of and precondition for
subsequent vascular damage by cholesterol. Research has further revealed that
cholesterol only becomes dangerous once it has been oxidised to oxycholesterol,
either in the diet or in vivo. This is brought about by the intervention of
free radicals. In this context it is particularly alarming that homocysteine
itself is a known stimulant for free radical induced oxidation of lipoproteins,
including that of cholesterol-rich lipoproteins, this besides other harmful
effects of free radicals in vivo. Moreover, in a manner to be explained further
below, thermally processed bottle feed products are themselves rich in
oxycholesterol but are deficient in counteracting substances present in human milk,

Even if the adverse factors described above, in particular elevated
homocysteine result in no immediately apparent symptoms, they may predispose to
atherosclerosis in later life.

The damage caused by homocysteine in infants is obviously not limited to the
vascular system but may include many other tissues and systems including the
central nervous system, which is particularly vulnerable at this stage.




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