As asked, I've investigated the research on fructose further, but I'm not
sure how applicable it is to the paleo diet with fruit. (I've omitted the
results relating to dental problems, gut intolerance and allergies.) The
results are also limited to human studies and English language. If you have
a specific disease or physiological process you would like me to research
further, let me know. From the results, it looks like Dr. Richard Bernstein
is correct in advising diabetics to limit or avoid fruit.

Authors
Teff KL.  Elliott SS.  Tschop M.  Kieffer TJ.  Rader D.  Heiman M.  Townsend
RR.  Keim NL.  D'Alessio D.  Havel PJ.
Institution
Monell Chemical Senses Center, University of Pennsylvania, Philadelphia
19104, USA.
Title
Dietary fructose reduces circulating insulin and leptin, attenuates
postprandial suppression of ghrelin, and increases triglycerides in women.
Source
Journal of Clinical Endocrinology & Metabolism.  89(6):2963-72, 2004 Jun.
Abstract
Previous studies indicate that leptin secretion is regulated by
insulin-mediated glucose metabolism. Because fructose, unlike glucose, does
not stimulate insulin secretion, we hypothesized that meals high in fructose
would result in lower leptin concentrations than meals containing the same
amount of glucose. Blood samples were collected every 30-60 min for 24 h
from 12 normal-weight women on 2 randomized days during which the subjects
consumed three meals containing 55, 30, and 15% of total kilocalories as
carbohydrate, fat, and protein, respectively, with 30% of kilocalories as
either a fructose-sweetened [high fructose (HFr)] or glucose-sweetened [high
glucose (HGl)] beverage. Meals were isocaloric in the two treatments.
Postprandial glycemic excursions were reduced by 66 +/- 12%, and insulin
responses were 65 +/- 5% lower (both P < 0.001) during HFr consumption. The
area under the curve for leptin during the first 12 h (-33 +/- 7%; P <
0.005), the entire 24 h (-21 +/- 8%; P < 0.02), and the diurnal amplitude
(peak - nadir) (24 +/- 6%; P < 0.0025) were reduced on the HFr day compared
with the HGl day. In addition, circulating levels of the orexigenic
gastroenteric hormone, ghrelin, were suppressed by approximately 30% 1-2 h
after ingestion of each HGl meal (P < 0.01), but postprandial suppression of
ghrelin was significantly less pronounced after HFr meals (P < 0.05 vs.
HGl). Consumption of HFr meals produced a rapid and prolonged elevation of
plasma triglycerides compared with the HGl day (P < 0.005). Because insulin
and leptin, and possibly ghrelin, function as key signals to the central
nervous system in the long-term regulation of energy balance, decreases of
circulating insulin and leptin and increased ghrelin concentrations, as
demonstrated in this study, could lead to increased caloric intake and
ultimately contribute to weight gain and obesity during chronic consumption
of diets high in fructose.

Authors
Vasdev S.  Longerich L.  Gill V.
Institution
Faculty of Medicine, Memorial University of Newfoundland, St. John's,
Newfoundland, Canada. [log in to unmask]
Title
Prevention of fructose-induced hypertension by dietary vitamins. [Review]
[124 refs]
Source
Clinical Biochemistry.  37(1):1-9, 2004 Jan.
Abstract
Essential hypertension in humans may develop through a combination of
genetic and environmental factors. Diet has long been under investigation as
a potential effector of blood pressure. A diet high in sucrose or fructose
can give rise to hyperlipidemia, insulin resistance and hypertension.
Insulin resistance, glucose intolerance and oxidative stress are common
features of hypertension. If glucose metabolism through the glycolytic
pathway is impaired, as in insulin resistance, there will be a build-up of
glyceraldehyde, glyceraldehyde-3-phosphate and dihydroxyacetone phosphate
with further metabolism to methylglyoxal, a highly reactive ketoaldehyde.
Excess aldehydes can bind sulfhydryl groups of membrane proteins, altering
membrane calcium channels, increasing cytosolic free calcium, peripheral
vascular resistance and blood pressure. The presence of reactive aldehydes
can also lead to oxidative stress. Dietary management through lower sucrose
or fructose intake and increas!
ed consumption of vitamins improves glucose metabolism, lowers tissue
aldehydes, increases anti-oxidant capacity and may also prevent
hypertension. [References: 124]

Authors
Pickering TG.
Institution
The Zena and Michael A. Wiener Cardiovascular Institute, Mt. Sinai School of
Medicine, 50 East 98th Street, New York, NY 10029-6574, USA.
Title
America the fat: fast food and fructose.
Source
Journal of Clinical Hypertension.  5(4):298-9, 2003 Jul-Aug.

Authors
Elliott SS.  Keim NL.  Stern JS.  Teff K.  Havel PJ.
Institution
Department of Nutrition, University of California, Davis 95616, USA.
Title
Fructose, weight gain, and the insulin resistance syndrome.[see comment].
[Review] [134 refs]
Source
American Journal of Clinical Nutrition.  76(5):911-22, 2002 Nov.
Abstract
This review explores whether fructose consumption might be a contributing
factor to the development of obesity and the accompanying metabolic
abnormalities observed in the insulin resistance syndrome. The per capita
disappearance data for fructose from the combined consumption of sucrose and
high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81
g/d in 1997. Both plasma insulin and leptin act in the central nervous
system in the long-term regulation of energy homeostasis. Because fructose
does not stimulate insulin secretion from pancreatic beta cells, the
consumption of foods and beverages containing fructose produces smaller
postprandial insulin excursions than does consumption of glucose-containing
carbohydrate. Because leptin production is regulated by insulin responses to
meals, fructose consumption also reduces circulating leptin concentrations.
The combined effects of lowered circulating leptin and insulin in
individuals who consume diets that are high in dietary fructose could
therefore increase the likelihood of weight gain and its associated
metabolic sequelae. In addition, fructose, compared with glucose, is
preferentially metabolized to lipid in the liver. Fructose consumption
induces insulin resistance, impaired glucose tolerance, hyperinsulinemia,
hypertriacylglycerolemia, and hypertension in animal models. The data in
humans are less clear. Although there are existing data on the metabolic and
endocrine effects of dietary fructose that suggest that increased
consumption of fructose may be detrimental in terms of body weight and
adiposity and the metabolic indexes associated with the insulin resistance
syndrome, much more research is needed to fully understand the metabolic
effect of dietary fructose in humans. [References: 134]

Authors
Howard BV.  Wylie-Rosett J.
Title
Sugar and cardiovascular disease: A statement for healthcare professionals
from the Committee on Nutrition of the Council on Nutrition, Physical
Activity, and Metabolism of the American Heart Association.[see
comment][erratum appears in Circulation. 2003 Apr 29;107(16)2166].
Source
Circulation.  106(4):523-7, 2002 Jul 23.