> I would be very interested to see the data that lactose enhances GI
permeability

Todd,

that lactose does something special with our gut must have been known for a
long time because I saw this mentioned in textbooks from the sixties
(without citations). But there are newer ones, too.

An experimental paper [1] concludes "These and other data indicated that
lactose is not interacting directly with Ca++ in solution but is
interacting with the absorptive cells of the intestine to increase
their permeability to Ca++."

There just was an interesting letter in the Journal of Pediatrics [2].
It should bee freely accessible online and has some citations.
If you shouldn't be able to find/read it, here are some of them: [3-5].

The paper [6] shows that lactose is not the only enhancing factor in milk.

Not every mineral uptake is enhanced [7,8],
and not only minerals are affected [9,10].

The uptake of intact IGF1 is another established fact [11,12].

I even remember an article showing that in humans, the blood levels of
IGF-1 after milk ingestion are elevated. Sorry, I lost the citation
(somewhere on my HD). Perhaps someone else knows it.

A close look at the original article [13] about that sialic acid (Neu5Gc)
raises some questions.

(i) The test persons avoided animal foods two days before the start of the
experiment and even avoided shampoos potentially containing Neu5Gc.(Good!)
Then they were given ~150mg Neu5Gc and continously fruit juice and soymilk
at a constant rate for 6 h. But as many foods of non-animal origin contain
milk sugar as an additive (possibly in the preexperimental period) and even
other sugars influence the uptake of nutrients [10] the Neu5Gc-uptake could
have been sustained as well. If there was a mild bowel inflammation in some
of the test persons caused by our western diet it might have persisted. The
guts of the volunteers should have been given a little more time to adapt
and a nutrition that heals inflammatory gut diseases.

(ii) The same authors made it likely [14] that the loss of the gene
responsible for Neu5Gc-formation in humans took place just before
the human brain startet to grow (and prey became the main food source).
They even suspect that this was a prerequisite for brain expansion in humans
because Neu5Gc-concentrations are always low in the brain even in animals
with high tissue levels of it. Neu5Gc seems to be well incorporated in
surface antigens of many human epithelial tissues after resorption [13]. As
such surface antigens are most likely involved in the recognition of our
"self" and in cellular communication this should happen under strong genetic
control and not by chance. And as Neu5Gc must have some function in animals,
we have to ask wether human tissues need it, too, at least in small amounts,
making it an essential nutritional factor and humans dependent on meat (like
with B12). Possibly, humans survived the loss of this sialic acid only
because they had food sources.
That it is found especially in tumor cells could even mean that these cells
switched off their control systems because the couldn't otherwise get enough
of it.
There is not a single aspect that supports a possible carcinogenicity of
Neu5Gc.

(iii) Even the presence of antibodies against Neu5Gc-containing
polysaccharides (pure Neu5Gc cannot be immunogenic) doesn't mean much. It
could simply be the consequence of a leaky gut permitting the uptake of
complex immunogenic substances thus leading to a mild form of "serum
sickness" [like mentioned in 13].
If they were directed against the Neu5Gc-containing human
antigens, they should have been extracted by our tissues [15].
There is a wide range of the measured antibody titers and they are small,
not like with the titers against the xenoantigen Gal-alpha1,3Gal.
Their Fig. 6 has different scale factors for both antibody-axes. All
Neu5Gc-titers are below the Gal-titers!
A reaction between such antibodies and our tissues would be some sort of
autoimmune reaction. A leaky gut could lead to the formation of
crossreacting autoantibodies.
But there are many epitopes in our nutrition which could do that under leaky
gut-conditions, even in vegetables.

roland


[1]Armbrecht, HJ, Wasserman RH.
Enhancement of Ca++ uptake by lactose in the rat small intestine.
J Nutr 1976 Sep;106(9):1265-71.

[2]J Pediatr 2003 Jun;142(6):737-8.

[3]Lengeman, FW.
The site of action of lactose in the enhancement of calcium utilization.
J Nutr 1959; 69: 537-546.

[4]Ziegler EF, et. al.
Lactose enhances mineral absorption in infancy.
J Pediatr Gastroenterol Nutr 1983; 2: 288-294.

[5]Moya M, et. al.
Short-term polycose substitution for lactose reduces calcium absorption in
healthy term babies.
J Pediatr Gastroenterol Nutr 1992; 14: 57-61.

[6]Camara-Martos F, et. al.
Influence of dietary factors on calcium bioavailability: a brief review.
Biol Trace Elem Res 2002 Oct;89(1):43-52.

[7]Abrams SA, et. al.
Calcium and zinc absorption from lactose-containing
and lactose-free infant formulas.
Am J Clin Nutr 2002 Aug;76(2):442-6.

[8]Beynen AC, et. al.
Magnesium balance in adult cats fed a dry food rich in lactose.
J Anim Physiol Anim Nutr (Berl) 2003 Aug;87(7-8):245-50.

[9]Lane RH, et. al.
IGF alters jejunal glucose transporter expression and serum glucose levels
in immature rats.
Am J Physiol Regul Integr Comp Physiol 2002 Dec;283(6):R1450-60.

[10]Play B, et. al.
Glucose and galactose regulate intestinal absorption of cholesterol.
Biochem Biophys Res Commun 2003 Oct 17;310(2):446-51.

[11]Philipps AF, et.al.
Absorption of milk-borne insulin-like growth factor-I into
portal blood of suckling rats.
J Pediatr Gastroenterol Nutr 2000 Aug;31(2):128-35.

[12]Buts JP.
Bioactive factors in milk
Arch Pediatr 1998 Mar;5(3):298-306.

[13]Ahead of print.
Tangvoranuntakul P, et. al.
Human uptake and incorporation of an immunogenic nonhuman dietary sialic acid.
PNAS 2003 Oct 14; 100: 12045-50.

[14]Chou HH, et. al.
Inactivation of CMP-N-acetylneuraminic acid hydroxylase occurred prior to
brain expansion during human evolution.
PNAS 2002 Sep 3;99(18):11736-41.

[15] Macchiarini P, et.al.
Evidence of human non-alpha-galactosyl antibodies involved in the
hyperacute rejection of pig lungs and their removal by pig organ perfusion.
J Thorac Cardiovasc Surg 1998 Nov;116(5):831-43.