Nutrition Flashcards

1
Q

Human Biology and Lifestyle Mismatch

A
  • Human biology is the product of evolution of millions of years
  • Earliest members of homo genus was 2 Mya
  • We are genetically adapted to the environment of our ancestors who foraged
  • 12,000 years ago: agriculture and farming caused a profound environmental change in diet and other lifestyle conditions which is a recent change
  • We evolved based on our ancestors 2 mya not our current times of agriculture and farming 12,000 years ago so mismatch
  • Mismatch pathway 1 – hunter gatherer to agriculture and farming causing overreliance
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2
Q

GI tract
- Australopithecines
- Homo genus

A
  • Australopithecines were herbivores
    o Ate fruits and tubers
    o Very long intestines with a large cecum to digest fiber
    o Late australopithecines may have scavenged for protein
  • Homo genus are omnivores
    o Fire for cooking so easier to chew/digest food
    o Smaller intestine to save energy & invest in increased brain size
    o Eating more energy rich meat so more energy for evolving brain
    o Appendix is an atavism (means no longer used), vestigial organ, used to digest cellulose
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3
Q

Appendicitis

A

appendix is easily infected because its no longer needed
o May be fatal so why hasn’t it been selected against
o Possibly rare until 19th century and then declined again so no time to be eliminated
o Infection
o Appendix is Left over from our past

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4
Q

Domestication of Fire
-functions

A
  • Fire was regularly used by: Neanderthals, erectus, sapiens
  • Functions
    1. Light, warmth, protection
    2. Torch areas to gather animals (hunt), harvest cooked animals and vegetables
    3. Cooking some foods that can only be digested after cooking so easier to chew, digest, metabolize
    o Wheat, tubers, rice
    o Killing germs and parasites (sterilize)
    o Eat more types of food
    o Spend less time eating = more efficient
    o Resulted in larger brains, shorter intestine and smaller teeth because no longer need to digest raw food
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5
Q

Fire and TB

A
  • Lesions on paleolithic humans and ancient DNA revealed the coevolution with mycobacterium tuberculosis
  • Most pathogens were transmitted from animals to humans but not TB
  • Mycobacteria live in soil and water theoretically but get burned in fire so in soot that is breathed in
  • Mycobacterium can cause opportunistic infections when infecting individuals with a weakened immune system
  • Fire in enclosed space lead to
    1. Smoke – inhaling smoke creates good environment for TB to grow
    2. Inflammation
    3. Bacterium spreads by coughing and sneezing
  • Coevolution with microbes = pathway #4
  • An environmental microbe that rarely causes disease evolved and specialized in becoming an obligate pathogen
    o A pathogen that cannot live outside of host
    o Fire gave mycobacterium the opportunity to spread in humans
    o Presence of inhaled smoke prevents the immune system from clearing lungs of pathogens
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6
Q

Tuberculosis

A
  • By beginning of 19th century TB had killed 1/7 of all people that had ever lived
  • Now affects ¼ of human population
  • Mycobacteria infect the lungs (90%) causing: chronic cough, blood containing sputum, fever
  • Extrapulmonary TB (10%) on skin: in immunocompromised individuals, lymphatic system, bones, CNS
  • Prophylaxis (prevention): vaccination
  • Treatment: antibiotics
  • Multiple strains of drug resistant TB now exist
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7
Q

Diet Evolution

A
  • A chimp spends ½ of his wakeful day chewing raw roots, fruits, leaves which requires extensive digestion
  • Australopithecines were vegetarian: wild plants like roots, fruits, leaves
  • Homo habilis became an opportunistic meat eater
  • Homo erectus: true hunter for 2 mya
  • Homo sapiens true mastery of fire
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8
Q

Human Diet
-5 lines of evidence

A
  • Humans have developed a greater brain mass and adapted the GI tract to provide an increased caloric intake: increased meat consumption
  • Lines of evidence
    1. Dental adaptations
    2. Skull adaptations
    3. Shorter GI tract
    4. Bone remains suggesting meat eating
    5. Anemia caused by lack of meat consumption
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9
Q

Dentition - line of evidence for Diet

A
  • Diet changes: herbivorous to omnivores
  • Smaller teeth
  • First molar in australopithecines = size of thumb nail
  • First molar in sapiens = size of pinky nail
  • Larger molars in herbivores and smaller in omnivores
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10
Q

Skull adaptations - line of evidence for Diet

A
  • In sapiens masseter & temporalis are smaller because reduce need to eat hard foods
  • Evidence by the origin and insertion sites on bone landmarks have changed because don’t chew as much
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11
Q

shorter GI tract - line of evidence for Diet

A
  • Most great apes have GI tract adapted to the digestion of foods that require extensive digestion: roots and leaves
  • Ape tract: stomach, appendix, colon are longer to process fibers
  • Modern humans have a significant reduction in gut size: a reduced need to digest fiber rich food and greater reliance on eating meat
  • More meat and fire use so less gut length needed
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12
Q

Bone remains suggest meat eating - line of evidence for Diet

A

Mammalian bones found in association with early H. habilis populations have cut marks and other evidence of butchery (use of tools) suggesting the consumption of meat

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13
Q

Anemia caused by lack of meat consumption - line of evidence for Diet

A
  • Shards of the skull of a 2 year old child were found in Olduvai Gorge in Tanzania
  • Possibly early homo habilis
  • The remains suggest the infant suffered from a form of malnutrition seen in meat poor diets = meat deficient anemia
  • The remains are dated 1.5 mya
  • The bones have porotic hyperostosis, a disease that typically results from a lack of vitamins B12 in the diet
    o Macrocytic anemia
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14
Q

Hosteoporosis symmetrica

A
  • Hosteoporosis symetrica is a pathological condition that affects bones of the cranial vault, and is characterized by localized areas of increased spongy or porous bone tissue
  • Is a result from the enlargement of hematopoietic marrow as a result of micronutrient deficiency anemia
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15
Q

Hematopoiesis

A
  • All blood cells are descended from a single precursor cell called pluripotent hematopoietic stem cell
  • In adults pluripotent hematopoietic stem cells are found primarily in red bone marrow
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16
Q

Hemoglobin in RBCs

A
  • Main function: transport O2 from lungs to tissues & CO2 from tissues to lungs
  • Tetrameric structure is made of: 4 hemes (prosthetic group) and 4 globin (protein)
  • Hemoglobin production requires various factors: iron (binds O2 in body), PLP (vit B6), zinc, nucleotides for proteins
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17
Q

Anemia
- cause
- symtpoms of severe anemia
- abnomalities in erythrocyte production
- 2 types

A
  • Cause: deficiency of RBC or hemoglobin or lack of things needed to make RBC or hemoglobin
  • Symptoms of severe anemia: fainting, chest pain, angina, heart attack
  • Abnormalities in the production of erythrocytes can be caused by:
    1. Insufficient cofactors (nutrient deficiency): vitamin B12, folate, iron
    2. Genetic abnormalities: congenital hemoglobinopathies (all heme disfunction in general), congenital membranopathies (shape of RBC), congenital thalassemia’s (quantity of globin produced)
  • 2 main types of anemia
    1. Increased destruction of RBC (hemolysis)
    2. underproduction of RBC
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18
Q

2 main types of anemia

A
  1. Increased destruction of RBC (hemolysis): leads to more immature RBCs because trying to create more RBCs to compensate for increased destruction
  2. Underproduction of RBC: leads to less production of immature RBC because of overall underproduction and there are three types
    o Microcytotic: MCV less than 80, less hemoglobin’s, iron/PLP/Zn deficiencies, thalassemia, microcytic anemia (small RBCs) caused by hemoglobin deficiency
    o Normocytic: b/w 80 & 100 MCV, acute blood loss, bone marrow disorder
    o Macrocytic: MCV over 100, characterized by nucleotide deficiency that causes macrocytic anemia (large RBC), B12 & folic acid deficiency
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19
Q

Macrocytic Anemia

A
  • RBCs are larger because of an impairment in DNA synthesis so the cell is stuck growing but cant divide (prevents cell cycle progression)
  • Cells stuck in G2 (growth) instead of progressing to M (replication)
  • But protein synthesis and other functions proceed unaffected resulting in larger cell size
  • Could be due to cobalamin or folate deficiencies because cant replicate with out nucleotides that are formed using cobalamin and folate
20
Q

Anemia & Micronutrient Deficiencies

A
  • Cobalamin and folate are required to synthesis DNA because they help create the nucleotides adenine, thymine,& guanine needed for DNA
  • Methyl cobalamin donates its methyl to THF (active form of folate) which in turn donates it to the nascent nucleotide
  • # 1 Source of cobalamin = beef = cow = liver
  • Recommended dietary allowance of cobalamin 2.6 (M) and 2.4 for Female and for folate 400 (male) and 600 (pregnant female)
21
Q

Microcytic Anemia

A
  • Iron deficiency causes: heme deficiency which in turn activates a feedback mechanism to inhibit globin and protein synthesis
  • iron deficiency = Not enough heme = stop protein& globin synthesis = cell stops growth = small RBC
  • No heme:
    1. Heme-regulated inhibitor (HRI) is active
    2. HRI phosphorylates the translation factor eIF2α
    3. P- eIF2α translation stops
    4. Small RBC size
22
Q

Iron Deficiency (general)

A
  • Most common nutritional deficiency in the world
  • 50% of anemia cases are attributed to iron deficiency
  • In advanced cases hypochromic microcytic anemia
  • Compensatory mechanisms
    o Less iron used by RBC
    o More iron available for other functions
    o Process mediated by iron regulatory proteins (IRP)
  • Several parameters of iron metabolism are evaluated
23
Q

Epidemic of Iron Deficiency

A
  • mothers need blood for growing fetus, and they can lose a lot of blood during birthing process
  • Consequences are devastating in children
    o Premature birth
    o Risk of infections
    o Cognitive development
    o Behavioral problems
  • Some people are to poor to eat meat so get iron deficiency anemia
24
Q

B12 & Fe Def Anemia

A
  • Both forms of anemia can be caused by lack of meat consumption
  • Our ancestors evolved to rely on meat consumption
  • H habilis was an opportunistic meat eater and H erectus were true hunters
  • Pathway #1: Mismatch between the environment we evolved in and current environment causes diseases
25
Q

Recent Transitions

A
  1. Neolithic revolution
    - Settlements lead to individual professions so society structure changed
    - Animal husbandry
    - Agriculture
    - Set stage for industrial revolution
  2. Industrial revolution
    - Nutritional abundance of modern societies
26
Q

Neolithic Revolution

A
  • Major turning point in human history
  • 13,000 years ago developed animal husbandry and agriculture
  • Radical change in human lifestyle from hunting/gathering which has sustained humans from earliest times
  • Food extraction (foraging) to food production (agriculture)
  • Societies grow and flourish, so population increases which led to individual professions leading to changes in societal structure (hierarchies develop)
  • Restricting food sources (over reliance on certain crops) led to famines and new diseases
27
Q

Nutrients changed from wild food to cultivated foods which had 3 effects

A
  1. Reduced variety of nutrients = potential for malnutrition and nutrient deficiency
    o Hunter gatherers relied on seasonal foods & ate what they found along their path
    o Ate wide variety of fruits, vegetables, roots, berries, seeds, nuts etc.
    o Nuts and roots were preserved
    o Fruit and vegetables consumed immediately
  2. Overreliance on crops = potential for famine
    o Irish famine only had one potato variety grown in the country so since potatoes reproduce asexually they all had the same genetics so no genetic variation so the blight spread and infected all potatoes which was a staple food of the poor and 1 million died and another 1 million fled
  3. Overcultivation = causes mineral depletion in the soil
    o caused by overcrowding in cities so constantly overuse land to feed growing population so soil & land less fertile & nutrient dense
    o continued cultivation of crops on same soil without additional input depletes the soil due to exhaustion of nutrients
    o causes: overpopulation, reduction of areas for agriculture, pesticides in the soil decreases quality of soil, increased productivity at expense of quality of food to make more money
28
Q

Nutrition Transition

A
  • initially agriculture populations were more prone to shortfalls in both energy and micronutrients as compared to foraging population, only recently with the nutrition transition we have achieved a greater degree of food security
  • in our society we have experienced remarkable nutritional abundance caused by economic demographic and epidemiological changes
29
Q

Industrial Revolution

A
  • 18th century
  • Agricultural revolution paved the way for industrial revolution which brought technological advances
  • Development of food processing procedures
  • New farming techniques and improved livestock breeding Led to amplified food production
  • Spike in population and increased health
  • New quantitative and qualitative food and nutrient combinations
  • Cheaper production of refined and processed foods
  • Intensive farming practices
  • Lucrative sale of nutrient poor food
  • Sugar could be addictive so people buy more food that’s bad for you
  • Overconsumption lead to decreased costs and increased availability of food with empty calories
  • Poverty = buy cheap empty calories bad food
30
Q

Food types introduced after agricultural and animal husbandry development

A

Dairy products, cereals, refined sugars, refined vegetable oils, and alcohol make up 72.1% of the total daily energy consumed in the US. Yet these types of foods would have contributed little or none of the energy in the typical preagricultural hominin diet

31
Q

history of refined sugars

A

First evidence of crystalline sucrose production appears about 500BC but before this honey was only form of concentrates sugar hominins could access and seasonal availability would have restricted access to sugar

32
Q

added sugars

A
  • Added sugars are refined forms of sugars that are artificially added in foods
  • Added sugars cause strain on pancreas and increase the odds of developing
    o Diabetes, Alzheimer’s, obesity, fatty liver disease, atherosclerosis, colon cancer
  • Natural sugar isn’t processed the same way as added sugar in the liver
33
Q

High Fructose Corn Syrup (HFCS)

A
  • Invention of chromatographic fructose enrichment tech in 70s allowed it to be economically feasible to manufacture high fructose corn syrup (HFCS) in mass quantity
  • Increased HFCS prevalence is worse than added sugar because it turns into triglycerides in the liver so more fatty liver disease
  • Fructose is metabolized in liver and converted into glycerol (backbone of triglycerides)
  • The accumulation of triglycerides in liver leads to development of fatty liver disease and insulin resistance
34
Q

alcohol

A
  • Alcohol consumption in US represents 1.4% of total energy consumed
  • Evidence of wine drinking in ancient times but incorporation of distilled alcohol beverages into human diet cam much later 800 to 1300AD
35
Q

Fatty liver disease (FLD) in general population prevalence

A
  • NAFLD prevalence in western countries 20-30%
  • Most common cause of chronic liver disease
  • NAFLD in 80-90% of obese adults
  • 30-50% in diabetic adults
  • 90% of patients with hyperlipidemia
  • Increasing prevalence of FLD
36
Q

Balance between triglyceride (TG) synthesis and removal

A
  • Steatosis = imbalance b/w TG synthesis and removal which leads to overproduction of TG and their accumulation in the liver
  • Fatty liver is common in Diabetics and starvation due to increased lipolysis in adipose tissue
  • Can be caused by excessive alcohol consumption
37
Q

Liver Disease Progression steps

A
  1. Healthy liver
  2. AFL/NAFL: steatosis (fat accumulation less than 5% of hepatocytes)
  3. ASH/NASH: steatohepatitis, so steatosis and inflammation and hepatocellular ballooning/injury
  4. Cirrhosis: liver tissue becomes fibrotic (scar tissue forms)
  5. Hepatocellular carcinoma
38
Q

Fatty Liver Disease

A
  • FLD is a broad spectrum of conditions caused by overnutrition (NAFLD) or alcohol consumption (AFLD)
  • Characterized by liver steatosis (accumulation of fat) with hepatocellular injury and inflammation
  • FLD is an Asymptomatic condition
  • Wide spectrum of liver damage caused by increased TG deposition in liver (NAFLD) and/or caused by the toxic effects of excessive alcohol consumption (AFLD)
  • FLD if TG in liver are above 5.5%
  • If TG accumulation happens then steatosis develops
39
Q

Steatohepatitis

A
  • TG accumulation within hepatocytes results in steatosis which increases the livers vulnerability to further injury
  • Primary lipotoxicity caused by oxidative stress from increased lipid peroxidation, high reactive oxygen species production within hepatocytes, mitochondrial dysfunction, and inflammation which all leads to cell death in liver
  • Damage to the liver causes progression to steatohepatitis
40
Q

Cirrhosis

A
  • Fibrosis: deposition of fibrous connective tissue like collagen (scar tissue) as a reparative response to injury or damage
  • Fibrosis can be a part of normal healing or to excess tissue deposition that occurs as a pathological process
  • Accumulation of fibrotic tissue leads to cirrhosis which impairs normal function of liver cells
41
Q

cereals and grains

A
  • Before Epi-Paleolithic there was little to no cereal grain consumption
  • Preceding industrial revolution: all cereals were ground with the use of stone milling tools and flour contained entire contents of the grains (germ, bran, endosperm)
  • Industrial revolution: invention of mechanized steel roller mills and automated sifting devices in the 19th century significantly altered the nutritional content of milled grain because they removed parts of the grain during process except for endosperm
  • 85.3% of cereals consumed the US diet are highly processed refined grains
  • ** haven’t consumed enough quantity of grain/wheat over evolutionary history but now recent introduction of it with agriculture and industrial revolution exponentially increase grain consumption so big evolutionary mismatch
42
Q

rice polishing

A
  • Polishing: removes husk (germ & bran layer) so removes proteins, vitamins, minerals, fiber, lipids
  • Complete milling and polishing of rice: removes B3, B1, B6, manganese, phosphorus, iron, dietary fiber, essential fatty acids
43
Q

Thiamin (B1) History

A
  • initially called thiamine but doesn’t have a amine group in it
  • deficiency is called Kakke’s in Japan in 17th century and considered a “national disease”
  • found predominantly in wealthy people because they ate polished rice mostly so poor nutrition so less nutrients
  • prevalent among people who ate white rice as staple in their diet
  • problem: amount and polishing of rice consumed
  • example of a cultural cause of a nutrient deficiency
44
Q

Beriberi

A
  • thiamin is necessary for metabolism for glycolysis
  • dry beriberi: related to peripheral nervous system
  • wet beriberi: related cardiovascular system
  • infantile beriberi: develops in infants breastfed by thiamin deficient mothers
  • due to fortification thiamin deficiency is rare in US but major groups at risk are
    1. alcoholics because destroy lining of jejunum so hard to absorb nutrients
    2. people on fad diets because restriction leads to nutrient deficiencies
    3. people on long term peritoneal or hemodialysis without thiamin replacement
    4. neonates breastfeeding from deficient mothers
45
Q

Dry Beriberi = peripheral nervous system involvement

A
  • thiamin plays pivotal role in neural function
  • peripheral neuropathy: impairment of sensory, motor, reflex functions of extremities
  • symptoms:
    o paresthesia (tingling)
    o burning sensation
    o muscle cramps
    o pain in legs
    o continued deficiency worsens peripheral neuropathy, often starts with legs then arms
    o associated with psychiatric problems like paranoia and hallucinations in advanced stages
46
Q

Wet Beriberi = cardiovascular

A
  • heart requires efficient cellular respiration so thiamin deficiency causes ATP depletion and leading to vasodilation, tachycardia, lactic acidosis
  • decreased BP promotes Renin-angiotensin-aldosterone system leading to sodium retention which in turn draws fluid in circulation and leads to edema
  • pedal edema: foot/ankle swelling is sign of heart failure