Journal Review of:

Appetitive, dietary and health effects of

almonds consumed with meals or as
snacks
By S.Y. Tan & R.D. Mattes

NTR 501
Metabolism
Emily Herrington
 The article that is being analyzed in this summary is Appetitive, dietary and health effects
of almonds consumed with meals or as snacks: a randomized, controlled trial that was published
by S.Y. Tan and R.D. Mattes on October 2nd, 2013. It was retrieved from the National Center for
Biotechnology Information, U.S. National Library of Medicine website on November 8, 2018.

The purpose of this study was to find the impact of almonds on health when consumed as
a snack. Snacking reportedly increases the risk for weight gain, but such a broad generalization
may mask differential responses to selected foods. This study compared post-ingestive and the
short-term effects of incorporating almonds in a meal or consuming them alone as snacks. It also
allowed the assessment of possible physiological adaptations to almond consumption that could
accentuate or diminish behavioral responses after 4 weeks of daily ingestion.

The methods for this study were as follows; Australian researchers S.Y. Tan and R.D.
Mattes recruited 137 subjects all who were at an increased for Type 2 diabetes based on their
being either overweight, obese or had normal weight with a strong family history for this disease.
They divided them into five groups, each of which was required to eat 43 grams (about 35
almonds or 262 calories) a day. The five groups were 1) Control Group, 2) a group that ate
almonds at breakfast, 3) a groups that had almonds at midmorning, 4) a group that had almonds
at lunch and 5) a group that had almonds as an afternoon snack. Participants (N=137) with
increased risk for type 2 diabetes completed an oral glucose tolerance test (OGTT) and acute-
feeding session at baseline, followed by almond consumption for 4 weeks before repeating the
OGTT and acute-feeding trials. Anthropometric, biochemical and appetite responses were
assessed.

The key findings of this article were that the almonds had a positive effect on subject’s
glucose and insulin levels. The most interesting results were seen in the “late afternoon” group,
though. The afternoon almond eaters had the greatest improvement in glucose and insulin levels
and they also lost fat, whittled away at their waistlines, and gained lean body mass. The
consumption of 43 g of almonds modulated postprandial glycemia and suppressed hunger and
desire to eat sensations especially after being consumed as snacks. The researchers could not
really explain why the afternoon snackers in particular exhibited increased lean body mass and
insulin responses superior to the other time. Over a 4-week period, almond consumption helped
meet recommended dietary intake of α-tocopherol and did not affect body weight (due largely to
strong dietary compensation) or postprandial lipid profiles in healthy adults at risk for type 2
diabetes (S.Y. Tan, 2013). The findings in this study suggests that almonds may be a healthy
snack option.

Key metabolic principles behind this study focused on lipid metabolism and fiber from
nuts. The serum glucose concentrations 60 min after breakfast and lunch meals were lower when
43 g of almonds were ingested with the meals. This may be attributable to the fiber and fat
content of almonds. Fiber reduces glycemia by increasing the viscosity of intestinal contents
hindering glucose diffusion, lowering the glucose concentration by reducing carbohydrate
availability in the gastrointestinal tract and capsulation of starch and hence impairing α-amylase
activity (S.Y. TaN. 2013). The researchers also believe fat derived from the almonds may have
caused lower postprandial glycemia by slowing gastric emptying times and dilution. The
glycemia-lowering-effect of fats is primarily due to a decreased absorption rate rather than an
increased clearance from the circulation as it takes fats longer to digest.

The pathways and mechanisms at play in this study starts with digestion and catabolism
of almonds and its nutrients. Fat breakdown starts in the stomach when the hormone gastrin
signals gastric glands to secrete gastric juice which has several components one being gastric
lipase which is an enzyme that helps to digest fat. Once fat molecules become micelles, lipases
go to work, breaking down fat molecules into fatty acids and monoglycerides, which pass
through the small intestine. After they pass through the small intestine, fatty acids are converted
to triglycerides, which combine with cholesterol, phospholipids and protein to form a structure
called a chylomicron (Gropper & Smith, 2013). The protein coating of the chylomicron makes it
water-soluble so it can travel through the lymph vessels and eventually the bloodstream. Once in
the circulation, they can either go to the liver or be stored in fat cells that comprise adipose tissue
found throughout the body.

Fatty acid metabolism consists of catabolic processes that generate energy, and anabolic
processes that create biologically important molecules. To obtain energy from fat, triglycerides
must first be broken down by hydrolysis into their two principal components, fatty acids and
glycerol. This process, called lipolysis, takes place in the cytoplasm. The resulting fatty acids are
oxidized by β-oxidation into acetyl CoA, which is used by the TCA Cycle. The glycerol that is
released from triglycerides after lipolysis directly enters the glycolysis pathway as DHAP.
Because one triglyceride molecule yields three fatty acid molecules with as much as 16 or more
carbons in each one, fat molecules yield more energy than carbohydrates and are an important
source of energy for the human body. Triglycerides yield more than twice the energy per unit
mass when compared to carbohydrates and proteins. Therefore, when glucose levels are low,
triglycerides can be converted into acetyl CoA molecules and used to generate ATP through
aerobic respiration.

The breakdown of fatty acids, called fatty acid oxidation or beta (β)-oxidation, begins in
the cytoplasm, where fatty acids are converted into fatty acyl CoA molecules. This fatty acyl
CoA combines with carnitine to create a fatty acyl carnitine molecule, which helps to transport
the fatty acid across the mitochondrial membrane (Gropper & Smith, 2013). Once inside the
mitochondrial matrix, the fatty acyl carnitine molecule is converted back into fatty acyl CoA and
then into acetyl CoA. The newly formed acetyl CoA enters the TCA Cycle and is used to
produce ATP in the same way as acetyl CoA derived from pyruvate. Almonds are a great source
of heart healthy monounsaturated fatty acids that go through this same process. Oleic acid is the
primary monounsaturated fat in almonds and it has been associated with a reduction in unhealthy
LDL cholesterol levels. Almonds’ nutrient profile has been praised for its health benefits and this
study proves that good fat sources are important for our health and they make a great snack
option as well.

References:

Gropper and Smith. (2013). Advanced Nutrition and Human Metabolism. 6th Ed. Wadsworth

Publishing.

Tan, S. Y., & Mattes, R. D. (2013). Appetitive, Dietary and Health Effects of Almonds Consumed

with Meals or as Snacks: a randomized, controlled trial. European Journal of Clinical

Nutrition, 67(11), 1205-14. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898316/