Chemistry Reference
In-Depth Information
carbohydrates and is modified by quantity, intrinsic orocecal transit time, which
delivers a certain amount across the ileocecal valve per unit time,
150
and by drugs
that prolong orocecal transit.
151
Symptoms of lactose maldigesters may also be exag-
gerated.
152
In Chinese participants (all LNP), intolerance or tolerance to lactose was
evaluated and found not to be related to fecal microbes or β-galactosidase,
153
and
was unrelated to alteration of oral cecal transit time.
154
As such, the mechanisms of
intolerance deserve further research.
It has now been established that the threshold dose for lactose digestion for a
single intake is between 6 and 10 g.
91,152,155-157
Above this threshold, lactose in LNP
subjects spills into the colon and bacterial metabolism becomes dominant. It was
found in a double-blind study comparing 3 day diet recall with response to a lac-
tose challenge that the pretest average daily lactose intake correlated in a dose-
response fashion with measured hydrogen response. A daily intake of greater than
20 g resulted in a sum of breath hydrogen that was significantly less than in subjects
who consumed 1 to 10 g/day.
158
Between 11 and 19 g, breath hydrogen sum was less
than the previous group, suggesting a dose effect. Regular lactose ingestion of 15 to
20 g/day may then be required to induce adaptation.
The adaptation to lactose has been observed in multiple epidemiological and
clinical studies.
159 -163
However, the formal description was clinically defined in a pro-
spective study by Hertzler and Savaiano,
164
where under test conditions LNP partici-
pants were shown to virtually change to LP phenotype.
164
In the original description,
the area under the curve for breath hydrogen was significantly reduced, symptoms
of intolerance improved, and fecal β-galactosidase increased about threefold from
baseline. Symptoms, especially gas and bloat, but also global effects, usually cor-
relate with the magnitude of the hydrogen response.
151,158,165
There has been some debate about whether improved symptoms found under
laboratory conditions after adaptation are due to a placebo rather than a true effect.
166
Indeed, functional (no clear disease-related symptoms) explanations for symptoms
of lactose intolerance are evident and severity may be overstated.
152
However, a pla-
cebo effect alone cannot explain all observations. If symptomatic improvement were
uniquely a placebo effect, it should be observed with other tested carbohydrates.
This is not the case with oligofructose and fructose itself.
167,168
In addition, symptoms
of lactose intolerance after pregnancy increase, corresponding to exacerbation or
unmasking of lactose maldigestion.
162
The effects of lactose on fecal microflora are also unclear. Following lactose
consumption,
in vitro
human fecal evaluation showed diminished hydrogen produc-
tion.
169
An increase in fecal β-galactosidase was shown, and this is interpreted as
either a population or metabolic expansion by bacteria. Because there is less hydro-
gen produced with adaptation, the suspicion of affected bacteria falls on lactic acid
producers, although some 80 percent of colonic bacteria have been found to possess
β-galactosidase.
170
The mechanism of adaptation is still not well defined. In a mouse
model, it was demonstrated that a lactose catabolizing strain of
Lactococcus lactis
was able to digest orally fed lactose.
171
This may not be the case in clinical stud-
ies, where mere expansion of fecal microflora with lactic acid (and yogurt) produc-
ing bacteria do not necessarily lead to improved lactose digestion.
172,173
In addition,
