Blood consumption

Is consumption of blood more "dangerous" compared to meat?

There was a news-article about unnatural chemicals found in the blood of mothers. This reminded me about a question I have pondered upon from time to time. Now, I am not a vampire, but curious as to the nature of blood vs meat in animals. More specifically unhealthy components.

There are various examples of viruses being in danger of spreading by consumption of raw blood like ebola, H5N1 etc. (But then also meat etc.)

Perhaps easier if I throw out some questions to show what I am asking:

  • Are there more of such in blood then meat?
  • Are there other things that can be worse in blood even after preparing? Like cooking, conservation etc.
  • Are parasites etc. more frequently found in blood?
  • Are there organisms that are highly resilient to heat treatment found in blood?
  • Are there more heavy metals in blood then meat? (Which I assume cooking does not give much of a difference.)
  • Other toxins?

Some references:

Is consumption of blood more "dangerous" compared to meat?

Actually yes, a simple high dose of blood is enough to kill. The cause is, though it is most important thing to live when flowing the vessel, it's highly toxic when consumed. There are high chances of getting haemochromatosis or Iron overload.

Source and More on this:

Composition of Blood


Blood Basics

Blood is a specialized body fluid. It has four main components: plasma, red blood cells, white blood cells, and platelets. Blood has many different functions, including:

  • transporting oxygen and nutrients to the lungs and tissues
  • forming blood clots to prevent excess blood loss
  • carrying cells and antibodies that fight infection
  • bringing waste products to the kidneys and liver, which filter and clean the blood
  • regulating body temperature

The blood that runs through the veins, arteries, and capillaries is known as whole blood, a mixture of about 55 percent plasma and 45 percent blood cells. About 7 to 8 percent of your total body weight is blood. An average-sized man has about 12 pints of blood in his body, and an average-sized woman has about nine pints.

The Components of Blood and Their Importance

Many people have undergone blood tests or donated blood , but hematology - the study of blood - encompasses much more than this. Doctors who specialize in hematology (hematologists) are leading the many advances being made in the treatment and prevention of blood diseases.

If you or someone you care about is diagnosed with a blood disorder, your primary care physician may refer you to a hematologist for further testing and treatment.


The liquid component of blood is called plasma, a mixture of water, sugar, fat, protein, and salts. The main job of the plasma is to transport blood cells throughout your body along with nutrients, waste products, antibodies, clotting proteins, chemical messengers such as hormones, and proteins that help maintain the body's fluid balance.

Red Blood Cells (also called erythrocytes or RBCs)

Known for their bright red color, red cells are the most abundant cell in the blood, accounting for about 40 to 45 percent of its volume. The shape of a red blood cell is a biconcave disk with a flattened center - in other words, both faces of the disc have shallow bowl-like indentations (a red blood cell looks like a donut).

Production of red blood cells is controlled by erythropoietin, a hormone produced primarily by the kidneys. Red blood cells start as immature cells in the bone marrow and after approximately seven days of maturation are released into the bloodstream. Unlike many other cells, red blood cells have no nucleus and can easily change shape, helping them fit through the various blood vessels in your body. However, while the lack of a nucleus makes a red blood cell more flexible, it also limits the life of the cell as it travels through the smallest blood vessels, damaging the cell's membranes and depleting its energy supplies. The red blood cell survives on average only 120 days.

Red cells contain a special protein called hemoglobin, which helps carry oxygen from the lungs to the rest of the body and then returns carbon dioxide from the body to the lungs so it can be exhaled. Blood appears red because of the large number of red blood cells, which get their color from the hemoglobin. The percentage of whole blood volume that is made up of red blood cells is called the hematocrit and is a common measure of red blood cell levels.

White Blood Cells (also called leukocytes)

White blood cells protect the body from infection. They are much fewer in number than red blood cells, accounting for about 1 percent of your blood.

The most common type of white blood cell is the neutrophil, which is the "immediate response" cell and accounts for 55 to 70 percent of the total white blood cell count. Each neutrophil lives less than a day, so your bone marrow must constantly make new neutrophils to maintain protection against infection. Transfusion of neutrophils is generally not effective since they do not remain in the body for very long.

The other major type of white blood cell is a lymphocyte. There are two main populations of these cells. T lymphocytes help regulate the function of other immune cells and directly attack various infected cells and tumors. B lymphocytes make antibodies, which are proteins that specifically target bacteria, viruses, and other foreign materials.

Platelets (also called thrombocytes)

Unlike red and white blood cells, platelets are not actually cells but rather small fragments of cells. Platelets help the blood clotting process (or coagulation) by gathering at the site of an injury, sticking to the lining of the injured blood vessel, and forming a platform on which blood coagulation can occur. This results in the formation of a fibrin clot, which covers the wound and prevents blood from leaking out. Fibrin also forms the initial scaffolding upon which new tissue forms, thus promoting healing.

A higher than normal number of platelets can cause unnecessary clotting, which can lead to strokes and heart attacks however, thanks to advances made in antiplatelet therapies, there are treatments available to help prevent these potentially fatal events. Conversely, lower than normal counts can lead to extensive bleeding.

Complete Blood Count (CBC)

A complete blood count (CBC) test gives your doctor important information about the types and numbers of cells in your blood, especially the red blood cells and their percentage (hematocrit) or protein content (hemoglobin), white blood cells, and platelets. The results of a CBC may diagnose conditions like anemia, infection, and other disorders. The platelet count and plasma clotting tests (prothombin time, partial thromboplastin time, and thrombin time) may be used to evaluate bleeding and clotting disorders.

Your doctor may also perform a blood smear, which is a way of looking at your blood cells under the microscope. In a normal blood smear, red blood cells will appear as regular, round cells with a pale center. Variations in the size or shape of these cells may suggest a blood disorder.

Where Do Blood Cells Come From?

Blood cells develop from hematopoietic stem cells and are formed in the bone marrow through the highly regulated process of hematopoiesis. Hematopoietic stem cells are capable of transforming into red blood cells, white blood cells, and platelets. These stem cells can be found circulating in the blood and bone marrow in people of all ages, as well as in the umbilical cords of newborn babies. Stem cells from all three sources may be used to treat a variety of diseases, including leukemia, lymphoma, bone marrow failure, and various immune disorders.

Where Can I Find More Information?

If you are interested in learning more about blood diseases and disorders, here are a few other resources that may be of some help:

The American Society of Hematology (ASH) Education Book, updated yearly by experts in the field, is a collection of articles about the current treatment options available to patients. The articles are categorized here by disease type. If you are interested in learning more about a particular blood disease, we encourage you to share and discuss these articles with your doctor.

Search Blood, the official journal of ASH, for the results of the latest blood research. While recent articles generally require a subscriber login, patients interested in viewing an access-controlled article in Blood may obtain a copy by e-mailing a request to the Blood Publishing Office.

This section includes a list of Web links to patient groups and other organizations that provide information.

Daily consumption of banana marginally improves blood glucose and lipid profile in hypercholesterolemic subjects and increases serum adiponectin in type 2 diabetic patients

In this study, we explored the effects of consumption of banana in thirty hypercholesterolemic and fifteen type 2 diabetic subjects. They were given a daily dose of 250 or 500 grams of banana for breakfast for 12 weeks. Fasting serum lipid, glucose and insulin levels were measured initially as well as every 4 weeks. Daily consumption of banana significantly lowered fasting blood glucose (from 99 ± 7.7 to 92 ± 6.9 and 102 ± 7.3 to 92 ± 5.7 mg x dL(-1) (p < 0.05) after consuming banana 250 or 500 g/day for 4 wk, respectively) and LDL-cholesterol/HDL-cholesterol ratio (from 2.7 ± 0.98 to 2.4 ± 0.85 and 2.8 ± 0.95 to 2.5 ± 0.79, p < 0.005) in hypercholesterolemic volunteers. Analysis of blood glycemic response after eating banana showed significantly lower 2 h-postprandial glucose level compared to baseline in hypercholesterolemic volunteers given a dose of 250 g/day. The changes of blood glucose and lipid profile in diabetic patients were not statistically significant, but for plasma levels of adiponectin, there were significantly increased (from 37.5 ± 9.36 to 48.8 ± 7.38 ngnml1, p < 0.05) compared to baseline. Although it remains to be confirmed with larger group of volunteers, this pilot study has demonstrated that daily consumption of banana (@ 250 g/day) is harmless both in diabetic and hypercholesterolemic volunteers and marginally beneficial to the later.

Blood consumption - Biology

The laboratory mouse, Mus musculus, belongs to the order Rodentia and family Muridae. The mouse is probably the most genetically and biologically characterized mammal in the world. Mice were first used for the study of respiration in the 17th century. Later in the 19th and 20th century they were bred for their coat color, and subsequently characterized genetically. Most of the common laboratory strains were developed in the early 1900s.

The mouse has short hair, a long naked tail, rounded erect ears, protruding eyes, a pointed snout and five toes on each foot. Mice come in a variety of colors. Insert picture of a mouse, get those cool ones.

Mice have a pair of incisors and three pairs upper and lower of molars. Molars are permanently rooted while the incisors have an open root and grow continuously. Due to this continuous growth of the incisors mice can have problems with overgrown teeth when the upper and lower incisors do not meet properly (malocclusion). Malocclusion can be hereditary or follow trauma, disease or inappropriate diet and/or soft food. There is no permanent cure for overgrown teeth the only treatment is to trim the teeth every 2-3 weeks, if malocclusion persists. Insert pictures.

Mice have a large horseshoe-shaped Harderian gland deep within the orbit. Secretions from the gland contain varying amounts of reddish-brown porphyrin pigment depending on the physiologic state, age, strain and sex of the mouse. The amount of secretions increases during stress and appears as 'red crusts' around the eyes and nostrils.

Normative Values for Mice

Males 20-30 g, Females 18-35g

Mice are communal animals, which live in a very hierarchical society. Within these groups they will aggressively defend their territories. Mums with newborns will likewise aggressively defend their pups and territories. Mice are nocturnal animals but adapt to their environments. While mice are timid, they may bite. Most of mouse behavior is pheromone driven.

Mice are communal animals with a social hierarchical system. This hierarchical system creates a situation whereby the dominant animals often barber (chew off the hair) those of lower rank. This behavior is especially evident among females and is more common in some strains than others. Subordinate animals may have their whiskers, trunk or flank hair removed. There are some suggestions that it may be a cooperative and/or learnt behavior. It appears to be of no sequelae for the health of the mice. Separating the dominant mouse often leads to rise of another dominant mouse. It is important that barbering is differentiated from other causes of hair loss or skin problems e.g. mites, fungi or bacteria by a veterinarian.

Mice have two distinct cervices and uterine bodies. There are separate urethral and vaginal openings. There is a vaginal closure membrane, which is lost at puberty. The inguinal canal remains patent throughout life. Mice have an os penis or os clitoridis associated with external genitalia.

Mice have a 4-5 day estrous cycle, divided into characteristic phases: proestrus, estrus and metestrus. The stage of the estrous cycle can be determined by vaginal cytology. Ovulation occurs at the end of metestrus. Mating leads to formation of a vaginal plug. Plugs persist for 16-24 hours and may last as long as 48 hours. Pregnancy lasts 19-21 days. Females will build a nest prior to parturition if opportunity is provided. Birth usually occurs at night with 10-12 pups being born. Stretching and hindleg extension are usually signs of impeding birth. Babies are born either head or tail first (breech). The female usually eats the placenta. Delivery lasts 1-4 hours, if labor persists call a veterinarian (5-3713). There is a fertile postpartum estrus. Maternal antibody is transferred to the fetus in utero and to the newborn via colostrum.

The young are born incompletely developed (altricius). They are born hairless and their eyes open after 10-12 days. Young are weaned after 21 days at which time they are 10-12 g. Puberty is attained at 4-6 weeks. Breeding onset is 7 weeks and breeding life is 7-9 months. It may be preferable to replace breeders when they are 6 months old.

Mice are generally fed a diet containing low fiber (5%), protein (20%) and fat (5-10%). Feed may be pelleted or powdered. The pelleted feed is supplied as regular, breeder, certified, irradiated or autoclavable. Mice are usually supplied feed free choice and they eat 4-5 g a day (12 g/100 g body weight/day). Water is supplied free choice and they usually drink 3-5 ml a day (1.5 ml/10 g body weight/day). Water may be supplied using a bottle or automatic waterers, and may be further treated by reverse osmosis, ozone, ultraviolet radiation, hyperchlorination or acidification. Picture caging, types of feed, feeders, watering systems

Mouse rooms are usually maintained at 30-70% relative humidity and a temperature of 18-26ºC (64-79ºF) with at least 10 room air changes per hour. The mice are housed in standard shoebox cages with or without filter tops. Filter tops prevent cross contamination of mice limiting the spread of disease and keep facilities clean. Cages with filter tops may have a slightly higher temperature, relative humidity, carbon dioxide and ammonia than the room air. Microisolator tops provide even a higher level of protection than bonnet type filter tops, since they seal better. Static cages as described above are usually changed one to two times a week depending on cage density and housing style. In ventilated cages air is forced into the cage at up to 60 air changes per hour. This keeps the cage dry and reduces build up of ammonia and carbon dioxide. In such situations cages are changed once every 1-2 weeks. Ventilated cages may be kept positive or negative to room air depending on the study being performed.

Mice are usually provided with some kind of bedding in the shoebox cages. Bedding can be paper, wood shaving, wood chips or corncob. In very rare instances mice are housed on wire floors.

Mice should always be clearly identified on cage cards indicating protocol number, strain, sex, age, supplier, investigator and contact person. Procedures performed on the animal should be clearly indicated. Individual mice can be identified using ear punches, ear tags, tattoos, fur dyes, indelible mark on tail or microchips. Picture with standard ear numbering.

Sex is determined using the anogenital distance. Males have a greater (1.5-2 times) anogenital distance than females as well as a larger genital papilla. In neonatal males the testis may be visible through the abdominal wall. Conspicuous bilateral rows of nipples are visible in females at about 9 days of age. Absence of testicles is not a useful criterion for sexing since the testis is retractable into the open inguinal canal throughout life.

Mice should be acclimatized to handling (gentling) to reduce stress. Always talk quietly, move hands slowly and handle them frequently. Mice should be handled at the base of the tail using your fingers or with forceps. Transfer the mice to a firm surface and apply a scruff hold to the loose skin between the ears with your fingers and forefingers while maintaining a grip on the tail. Do not pull the skin too tightly as the mice can choke, too loose a hold will allow the mouse to turn its head and bite. This hold allows you to examine the under belly and perform other procedures. A variety of restraint devices are available to assist in handling mice.

Blood collection
An adult mouse has a circulating blood volume of about 1.5-2.5 ml (6-8% of the body weight), however in older and obese animals this may be lower. Up to 10% of the circulating blood volume may be taken on a single occasion from a normal healthy animal on an adequate plane of nutrition with minimal adverse effect. Always make sure the animal has recovered safely from the procedure and give warm isotonic fluids. This volume may be repeated after 3-4 weeks. For repeat bleeds at shorter intervals, a maximum of 1% of an animal's circulating blood volume can be removed every 24 hours.

Blood can be collected from several sites in the mouse including tail vein, saphenous vein, retro-orbital sinus, brachial vessels, vena cava or cardiac puncture. Always ensure complete hemostasis before returning the mouse to its home cage.

It may be necessary to warm the tail by exposing it briefly to a heat lamp or placing it in a bowl of warm water. The mouse should be restrained in a device for the collection. Blood can be collected from the tail vein (and artery) by making a snip in terminal =3 mm of the tail with a scalpel or sharp scissors. Stroke the tail gently with thumb and finger to enhance flow of blood into the collection vial. Because of the thermoregulatory function of the tail no more than the distal 3 mm should be taken at a time. At the end of the collection apply pressure to the cut end with a gauze bandage and ensure that blood has completely stopped flowing before returning the mouse to the cage. A small nick can also be made at side of the tail 0.5 -2cm from the tail base to collect blood. A fine gauge needle introduced through the skin at a shallow angle can be used to withdraw blood from the tail vein. Apply a tourniquet around the base of the tail to aid in the collection. A butterfly catheter with only about 5 mm of tubing attached to it (rest cut off) may be used instead of a needle and syringe.

Saphenous vein

Restrain and extend the hind leg applying gentle downward pressure above the knee joint. This stretches the skin making it easier to shave and immobilizes the saphenous vein. Wipe the shaved area with alcohol or sterile lubricate gel and use a 25-gauge needle to puncture the vein (Vein is highlighted by the dark line in the picture below). If done correctly a drop of blood forms immediately at the puncture site and can be collected in a microhematocrit tube. Gentle pressure over the puncture site or relaxation of the restrainer's grip is usually sufficient to stop the blood flow. The scab at the puncture site can be rubbed off at a later date to allow additional blood collection.

Retrorbital sinus
The retrorbital sinus is a system of dilated venous channels at the back of the orbit. Blood can be collected form this area in anesthetized mice using a microhematocrit tube. There should be no movement of the head during the procedure. Pressure down with the thumb and forefinger just behind the eye and pull back on the skin to allow the eyeball to protrude. Position a microhematocrit tube along the inner corner of the eye (medial canthus) beside the eyeball. Insert the tube gently but firmly through the conjunctiva towards the back of the eye along the orbit. Rotate the tube gently as you proceed. Blood should flow freely, if, the tube is properly inserted. Tilt the head slightly downward to improve flow. After collecting the blood withdraw the tube and apply pressure on the closed eyelids to stop any bleeding. Remove excess blood with gauze. Complications include damage to the eye and surrounding tissues.

Brachial vessels
Blood can be collected from the brachial plexus as a terminal procedure in deeply anesthetized mice. Make a cut through the skin at the side of the thorax into the angle of the forelimb (axilla) to expose the axillary vessels. Transect the vessels and allow blood to pool into the pocket created by tenting the skin. Aspirate the mixed venous arterial blood is into an appropriate receptacle.

Vena cava and abdominal aorta
Blood can be obtained from the posterior vena cava or abdominal aorta in a deeply anesthetized mouse following laparotomy. Approach the vessel at a shallow angle using a fine gauge needle attached to a small syringe. This is a terminal procedure.

Cardiac puncture
Up to 1 ml of blood can be obtained from the heart of a deeply anesthetized mouse in a terminal procedure. The most common approach is to lay the mouse on its back and insert a 25 to 30 gauge needle attached to a 1ml syringe just behind the xiphoid cartilage and slightly left of the middle. The needle should be introduced at 10-30 degrees from the horizontal axis of the sternum in order to enter the heart. Alternatively approach the heart laterally immediately behind the elbow at the point of maximum heartbeat.

Administration of substances

Materials to be administered to mice can be given orally e.g. in water or feed or injected systemically through a variety of routes. The average daily consumption of feed and water for an adult 25 g mouse is 3-5 g and 4 ml respectively. The following volumes can be injected into mice safely (based on 25 g mouse): 2-3 ml subcutaneously, 0.05-0.1 ml intramuscularly (0.03 ml per site), 0.50 ml intravenously, 0.1-0.3 ml into the stomach and 2-3 ml intraperitonealy. Intramuscular injections are usually not recommended in mice because of the small muscle mass. A fine gauge needle should be used to make injections in the anterior thigh muscle. It is good practice to use a new needle each time you perform an injection.

Oral gavage is performed using a ball ended feeding needle. Estimate the distance that the needle needs to be inserted into the mouse (usually from the nose to the first rib) and mark it on the needle. Restrain the mouse with the head and body extended as straight as possible to facilitate introduction of the gavage needle. Introduce the needle in the space between the left incisors and molars, and gently direct it caudally toward the right ramus of the mandible. The mouse usually swallows as the feeding tube approaches the pharynx, facilitating entry into the esophagus. If the animal struggles or appears to be in respiratory difficulty withdraw the tube and begin all over again. Once the desired position is attained, inject the material and withdraw the syringe. Monitor the animal after the procedure to ensure that there are no adverse effects.

Subcutaneous injections
Subcutaneous injections are usually made into the loose skin over the neck or flank using a fine gauge needle. Insert the needle 5-10 mm through the skin before making the injection. Lack of resistance to the injection is indicative that you are in the right location. Check for leak back especially if a larger volume is injected.

Intraperitoneal injections
Intraperitoneal injections are usually made in the lower right quadrant of the abdomen. The mouse is restrained with its head tilted lower than the body to avoid injury to internal organs. After swabbing the lower right quadrant with alcohol, a fine gauge needle is introduced slowly through the skin, subcutaneous tissue and abdominal wall. Withdraw the syringe plunger to ensure that you are not in the bladder or intestines. If nothing is withdrawn inject the material slowly. If you accidentally enter the bladder or intestines withdraw and discard the needle and syringe.

Intravenous injections
Intravenous injections are usually made into the dorsal tail vein. Warm the tail by immersing it in warm water or placing the animal under a heat lamp. The tail vein is easier to see in non-pigmented mice. A fine gauge needle should be used for this procedure.

Signs of pain in the mouse

Pain relief
For a detailed discussion of pain relief in mice refer to module 2. Generally opioids e.g. buprenorphine or non-steroidal anti-inflammatory agents e.g. acetaminophen, ketoprofen, caprofen, ibuprofen are used to relieve pain. Drugs can be administered in water, in jello, as oral drops, by gavage or injected. Drugs administered in water may be broken down in water, or insufficient quantities may be taken due to poor solubility in water or palatability problems.

In general inhalant anesthetics are safer than injectable anesthetics. Halothane and isoflurane are the safest ones to use. Methoxyflurane is no longer available. Use of ether at Johns Hopkins University is subject to restrictions due to safety concerns. Ketamine and xylazine is a common injectable anesthetic combination. Sodium pentobarbital can be used, but it has a narrow safety margin and is associated with a prolonged recovery period. For details on anesthetic techniques refer to the rodent surgery module.

Euthanasia in mice is most often performed by carbon dioxide asphyxiation or overdose of an anesthetic agent. Use of cervical dislocation or decapitation in absence of deep anesthesia must be scientifically justified. All individuals performing euthanasia must be properly trained. Individuals must also ensure that animals are dead before the carcass is disposed. Exsanguination or opening the thoracic cavity will ensure death. AVMA Panel on euthanasia report

Diseases of mice are usually handled as a herd (colony) health problem rather than on an individual animal basis. The goal is to prevent introduction of a disease into a colony rather than to treat animals after disease outbreak. Disease prevention is practiced by institution of a disease surveillance (sentinel) program based on serological and microscopic diagnosis of problems in a representative sample of animals. Due to the widespread movement of animals all over the world with advent of genetic manipulation of animals, the possibility of introducing disease agents in a colony has markedly increased. The expanded use of genetically modified and immunocompromised animals greatly exacerbates the problem. Furthermore the practice of transplanting tumor material into mice provides a portal where these agents can be introduced into animal, especially if the tumors are not screened for adventitious infectious agents. Some important mouse diseases are discussed below to draw attention to the need to adhere to practices recommended by the veterinary staff to avoid these diseases.

Pinworms (Syphacia and Aspicularis) inhabit the intestine (cecum, rectum, colon) and have a direct lifecycle. The eggs are particularly resistant and survive for a long time in the environment. The disease is usually subclinical being marked in weanlings and immunocompromised animals. Symptoms include poor body condition, rough hair coat, reduced growth rate and rectal prolapse. Infection with pinworms has a negative impact on gastrointestinal, growth, behavioral and immunology studies.

Mites affect the skin of mice and up to 100% of the animals may be affected. Affected animals are scruffy, pruritic (itchy), loose hair and have scratch wounds, which can become infected with bacteria. There are changes in the immune responses of affected animals.

Mouse hepatitis virus
This is a viral disease of mice that affects multiple organs. Weanlings are important in maintaining the disease in a colony. Outbreaks result in widespread deaths in neonates and occasionally weanlings, with or without diarrhea. Mouse hepatitis virus causes a wasting disease and high mortality in immunocompromised animals. Usually 100% of the animals are infected. This disease wreaks havoc in a colony, with disruption in research especially in oncology, transplantation, immunology, gastroenterology, metabolism and transgenic technology.

This viral disease is the worst nightmare in a mouse colony. There have been recent outbreaks at several facilities in United States associated with the injection of mouse sera or tissue culture material containing mouse sera into mice. The disease produces massive die off in adult mice and amputation of the limbs (ectromelia) in surviving animals. Pox lesions (mousepox) appear on the skin. There is conjunctivitis, hair loss, as well as swelling of the liver, spleen and lymph nodes. Ectromelia causes high mortality and drastic measures including depopulation are usually taken to eliminate the disease.

This is a fungal disease affecting a wide range of laboratory animals and humans. The organisms are primarily localized in the lungs but may also involve other organs including the eyes, skin etc. It causes a slowly progressive chronic pneumonia with weight loss and eventually death in a large number of immunocompromised animals. The disease has a severe negative impact in research involving immunocompromised animals, pulmonary function and immunology.

Causes of Vasodilation


Vasodilation can occur due to endogenous (internal) or exogenous (external) factors. Chemicals, hormones, and nerves are all endogenous factors that cause vasodilation. Increased levels of carbon dioxide, potassium ions, hydrogen ions, and adenosine, along with an increase in the osmolarity of the extracellular fluid, can all cause vasodilation. The hormone epinephrine (adrenalin) can cause activation of beta-2 receptors in the blood vessels in muscles to allow them to dilate during exercise. Nitrous oxide is another substance released by certain nerves that is a vasodilator. It is released during inflammation and also plays a role in regulating respiratory and digestive functions.

If a blood vessel is constricted for too long and then released, there will be increased blood flow afterwards. This is called reactive hyperemia. It can occur in people with Raynaud syndrome, who often have reduced blood flow due to arterial spasms and then subsequently have increased blood flow that can cause redness and pain. Reactive hyperemia can also occur from endogenous factors, such as if a blood pressure cuff is left on the arm for too long.


Certain foods and beverages cause vasodilation, such as capsaicin (found in chili peppers) and alcohol. This is why people can appear flushed after consuming these substances. Other factors such as light and noises in the environment can also play a role in vasodilation. When there is a lot of light or environmental noise, vasoconstriction occurs, but when high levels of these factors are absent, vasodilation will occur.

Some pharmaceutical drugs are vasodilators and used for the treatment of conditions like hypertension (high blood pressure), congestive heart failure, chest pain, and erectile dysfunction. One side effect of medications that are vasodilators is becoming flushed, which is what we have previously seen can also occur from other endogenous vasodilators. Some vasodilators only dilate arteries, some dilate veins, and some dilate both. The type of vasodilator given depends on the medical condition for example, venous vasodilators are effective in treating chest pain caused by angina, but are ineffective for treating hypertension since they do not also dilate arteries. Some vasodilators have other beneficial functions in addition to dilating blood vessels. Calcium channel blockers, for example, can help regulate arrhythmias of the heart in addition to lowering blood pressure.

Diagnosis - Disseminated Intravascular Coagulation

Your doctor will diagnose DIC based on your medical history, a physical exam, and tests. Your doctor will also look for the cause of DIC, because it does not occur on its own.

To help diagnose DIC, your doctor will ask about any medical conditions or recent events, such as illness or an injury, that could cause or be a risk factor for DIC. Your doctor will do a physical exam to look for signs and symptoms of blood clots, bleeding, or a condition that could cause DIC or a complication of DIC.

If your doctor suspects DIC, the following blood tests may help diagnose it:

  • Blood clotting tests, such as prothrombin time (PT) and partial thromboplastin time (PTT), to measure how well and how long it takes your blood to clot. If you have DIC, your clotting time may be longer than normal.
  • Complete blood count (CBC) to measure the number of red blood cells, white blood cells, and platelets in your blood. If you have DIC, the numbers of platelets, red cells, or both may be low.
  • Comprehensive metabolic panel (CMP) to measure your kidney function, liver function, and the sugar and electrolyte levels in your blood. Abnormal results could indicate that DIC caused damage to your kidneys or liver or could identify another underlying condition that caused your DIC.
  • D-dimer tests to look for blood clots. The test measures D-dimer, a substance that is released in the blood when blood clots dissolve. D-dimer levels may be high if you have DIC.
  • Peripheral blood smear to look at the number, size, and shape of your platelets and other blood cells. In a peripheral blood smear, a small amount of your blood is examined under a microscope. The presence of damaged red blood cells may suggest DIC.
  • Serum fibrinogen tests to measure how much fibrinogen is in your blood. Fibrinogen is a protein that helps the blood clot and may be low if you have DIC.

Your doctor may use a scoring system to diagnose DIC. The score is based on your platelet count, PT, D-dimer test, and fibrinogen levels. The higher the score, the more likely it is that you have DIC. To make a diagnosis, your doctor may repeat some tests and monitor your condition over time.

Your doctor may suggest additional tests or procedures to find out whether another condition is causing your symptoms. These tests may include:

  • ADAMTS13 testing to check blood levels and activity of this protein, which is low in thrombotic thrombocytopenic purpura (TTP), a type of platelet disorder
  • Liver biopsy and liver function tests to check for cirrhosis or chronic liver disease, which may have signs and symptoms that are similar to DIC
  • Return to Risk Factors to review how infection, injury, lifestyle, or other medical conditions may increase your risk of developing DIC.
  • Return to Signs, Symptoms, and Complications to review common signs and symptoms of DIC.

Metabolomics and proteomics as tools to advance the understanding of exercise responses: The emerging role of gut microbiota in athlete health and performance

Caimari Antoni , . Francesc Puiggròs , in Sports, Exercise, and Nutritional Genomics , 2019

19.2.2 PTMs of key proteins of energy metabolism in response to physical exercise

Energy metabolism is the process of generating energy (ATP) from nutrients and comprises a series of interconnected pathways that can function in the presence or absence of oxygen. Aerobic metabolism converts one glucose molecule into 30–32 ATP molecules. Fermentation or anaerobic metabolism is less efficient than aerobic metabolism.

Exercise is intrinsically related to energy metabolism ( Westerterp and Plasqui, 2004 ), and one way cells solve the increased energy demand during exercise is by ramping up the synthesis of mitochondria, the cells’ power generators. Because mitochondria are the major regulators of cellular energy metabolism, providing the vast majority of ATP for cellular activity, mitochondrial dysfunction has been linked to the pathogenesis of some metabolic disorders, including obesity and type II diabetes mellitus (T2DM) ( Boudina et al., 2005 Bugger et al., 2010 ). Therefore, it is important to identify the factors that control mitochondrial function and energy metabolism and that regulate the adaptive metabolic responses required by the increasing energy demands associated with exercise.

Several studies have analyzed the effect of an exercise period on the expression pattern and PTM of multiple protein classes and revealed that approximately 90% of the proteins identified were associated with energy metabolism, comprising enzymes involved in glucose catabolism, ATP synthesis and glutamate turnover ( Ding et al., 2006 ).

The catalytic capacity of an enzyme can be changed by the noncovalent binding of allosteric effectors and/or by covalent PTMs, which involves an alteration of the original chemical composition of a protein after its translation. During the PTM process, biochemical groups, such as acetyl, phosphate, methyl, ubiquitin, and various lipid and carbohydrate residues, can be attached to or removed from specific amino acids in proteins. PTMs are one of the most important mechanisms for activating, changing or suppressing protein functions and represent an important way to diversify and regulate enzymatic activity ( Walsh et al., 2005 ). It is a well-orchestrated process because each PTM requires a specialized protein that catalyzes the particular modification, and some are reversible by the action of a specific protein.

Focusing on the most important PTM associated with the adaptive metabolic responses to acute exercise, a list of phosphorylated, acetylated, and ubiquitinated proteins will be described hereafter.

Phosphorylation—During muscle contraction, a number of stressors are induced (increased AMP/ATP ratio, ROS and lactate generation, Ca 2 + flux, hypoxia, decreased energy availability) and collectively alter the posttranslational status of key cell signaling kinases. In the first global analysis of the phosphoproteome of human skeletal muscle in healthy subjects, 367 phosphorylation sites in 144 phosphoproteins were described. More than one-quarter were sarcomeric proteins from the contractile apparatus. Other phosphorylation sites were identified in some enzymes of glycogen metabolism and in some kinase and phosphatase subunits that regulate the phosphorylation of glycogen synthase and glycogen phosphorylase ( Lundby et al., 2012 ). In mitochondria, other authors identified 155 distinct phosphorylation sites in 77 mitochondrial phosphoproteins that are mainly involved in oxidative phosphorylation (OXPHOS) (the most abundant), the TCA cycle, fatty transporters, β-oxidation, amino acid degradation, import machinery and transporters, calcium homeostasis, and apoptosis ( Zhao et al., 2011 ). A recent global phosphoproteomic analysis of human muscle in response to a single bout of intense exercise (10 min cycling at 90% of V̇O2 max) revealed 1004 unique exercise-regulated phosphosites on 562 proteins, including substrates of known exercise-regulated kinases [such as AMP-dependent protein kinase (AMPK), protein kinase A (PKA), calcium/calmodulin-dependent protein kinase (CaMK), mitogen-activated protein kinase (MAPK), and mammalian target of rapamycin (mTOR)], although the majority of these targets had not been previously related with exercise signaling ( Hoffman et al., 2015 ).

The acute PTMs of cellular signaling kinases, such as CaMKII, p38MAPK, and AMPK, acting alone or in combination with each other, can subsequently activate downstream transcription factors and coactivators that exert regulatory roles in the coordination of the expression of both nuclear and mitochondrial-encoded proteins, such as the peroxisome proliferator-activated γ receptor coactivator (PGC-1α) ( Egan et al., 2010 ). PGC-1α, the so-called ‘master regulator’ of mitochondrial biogenesis, triggers pathways that promote mitochondrial synthesis and regulate both mitochondrial activity and energy metabolism ( Liang and Ward, 2006 ). The phosphorylation of PGC-1α on different sites results in increased activity and subsequent translocation into both the nucleus ( Little et al., 2010 ) and mitochondria ( Safdar et al., 2011 ) during acute exercise, where it recruits and coregulates multiple transcription factors that control skeletal muscle gene expression, including nuclear respiratory factor 1 (NRF-1), nuclear respiratory factor 2 (NRF-2), estrogen-related receptor alpha (ERRα), and mitochondrial transcription factor A (TFAM) ( Egan and Zierath, 2013 Hawley et al., 2014 ).

Additionally, acute exercise also induces phosphorylation of the p53 protein, a potent regulator of mitochondrial content, function, and biogenesis ( Bartlett et al., 2014 ). The phosphorylation of p53 on serine 15, typically associated with increased stability and activity, occurred in parallel with the classical exercise-induced phosphorylation of both AMPK and p38MAPK, thus suggesting that these kinases may serve as upstream kinases modifying p53 activity.

Acetylation—A proteomics study in mouse liver mitochondria comparing sedentary, forced endurance exercise, and forced endurance plus 3-h recovery groups identified 277 acetylation sites on 133 mitochondrial proteins ( Safdar et al., 2011 ). Deacetylases play an important role in energy metabolism. One of the well-established Sirtuin 1 (SIRT1) metabolic substrates is PGC-1α, which when it is deacetylated and activated, leads to a transcriptional switch from glycolytic to gluconeogenic genes in the liver and thus increases hepatic glucose production. In the liver and skeletal muscle, deacetylation of PGC-1α by SIRT1 induces the gene expression of fatty acid oxidation enzymes, and in a fasted liver, this deacetylation shifts the fuel usage from glucose to fatty acids ( Gerhart-Hines et al., 2007 ).

SIRT1 also deacetylates other transcription factors, such as forkhead box protein O1 (FOXO1) and signal transducer and activator of transcription 3 (STAT3). Deacetylation of FOXO1, a crucial mediator of whole-body energy metabolism, activates target genes involved in gluconeogenesis in hepatocytes ( Rui, 2014 ). Considering that PGC-1α serves as a coactivator for FOXO1, the deacetylation of both PGC-1α and FOXO1 by SIRT1 might have synergistic effects on their common gluconeogenic target genes. The transcription factor STAT3 acts as a negative regulator of gluconeogenesis, suppressing PGC-1α expression and thus inhibiting gluconeogenesis in the liver. The deacetylation of STAT3 by SIRT1 inhibits its phosphorylation and its translocation into the nucleus where it represses PGC-1α expression, and its suppression of gluconeogenesis is relieved ( Nie et al., 2009 ).

Ubiquitination—Another important PTM that regulates mitochondrial energy metabolism is the ubiquitin-dependent degradation of mitochondrial proteins. The turnover of several OXPHOS proteins is dependent on the ubiquitin-proteasome system (UPS). Specifically, UPS-dependent degradation of succinate dehydrogenase subunit A (SDHA) promotes SDHA-dependent oxygen consumption and increases ATP, malate, and citrate levels ( Lavie et al., 2018 ). A study performed in men exposed to divergent modes of exercise training and a single bout of exercise performed in the trained state demonstrated that prolonged traditional endurance and resistance training would both stimulate upregulation of basal levels of UPP molecular markers as a mechanism of muscle remodeling to maintain an optimal size of the type I fibers. These results suggest that adaptations due to endurance exercise training are more reliant on protein UPP degradation processes than adaptations due to resistance exercise training.

Biology Chapter 8

A. They are long, thin appendages that allow bacteria to be motile (move).
B. They are stiff fibers that allow bacteria to adhere to surfaces.

A. Plasmids and antibiotic resistance.

B. A peptidoglycan cell wall.

C. An outer membrane composed of lipopolysaccharide.

A. an opportunistic infection.

A. because they do not replicate

B. because they do not possess genetic material

C. because they are not composed of cells

D. because they lack the metabolic machinery to acquire and use nutrients

D. opportunistic infections.

A. helper T cells and macrophages

B. B cells and red marrow cells

C. liver cells and cardiac muscle cells

D. epithelial cells and eosinophils

D. opportunistic infection

A. It can infect any cell it comes in contact with.

B. It can only infect cells on surfaces of the body where the temperature is lower.

C. It can only infect cells that are actively growing and dividing.

A. because there is no HIV in the blood

B. because there are no detectable levels of HIV antibodies in the blood

B. yeast infections of the mouth or vagina

A. the destruction of CD4 T cells by the virus

B. the production of new CD4 T cells

C. the amplification of the virus in the blood

D. the destruction of the virus by the immune system

2. Fusion: HIV fuses with the plasma membrane, and the virus enters the host cell.

3. Entry: The capsid and protein coats are removed, releasing RNA and viral proteins into the host cell's cytoplasm.

4. Reverse transcription: HIV's single-stranded RNA is converted into a double-stranded viral DNA code.

5. Integration: The viral DNA, along with the viral enzyme integrase, migrates into the nucleus of the host cell. The viral DNA is spliced into the host cell's DNA, making it part of the host genome.

6. Biosynthesis and cleavage: The host cell's machinery directs the production of more viral RNA. Some of the viral RNA becomes material for new viruses, while the rest is used to code for viral proteins.

7. Assembly: Capsid proteins, viral enzymes, and RNA are assembled into new viruses.

Blood components

In humans, blood is an opaque red fluid, freely flowing but denser and more viscous than water. The characteristic colour is imparted by hemoglobin, a unique iron-containing protein. Hemoglobin brightens in colour when saturated with oxygen (oxyhemoglobin) and darkens when oxygen is removed (deoxyhemoglobin). For this reason, the partially deoxygenated blood from a vein is darker than oxygenated blood from an artery. The red blood cells ( erythrocytes) constitute about 45 percent of the volume of the blood, and the remaining cells (white blood cells, or leukocytes, and platelets, or thrombocytes) less than 1 percent. The fluid portion, plasma, is a clear, slightly sticky, yellowish liquid. After a fatty meal, plasma transiently appears turbid. Within the body the blood is permanently fluid, and turbulent flow assures that cells and plasma are fairly homogeneously mixed.

The total amount of blood in humans varies with age, sex, weight, body type, and other factors, but a rough average figure for adults is about 60 millilitres per kilogram of body weight. An average young male has a plasma volume of about 35 millilitres and a red cell volume of about 30 millilitres per kilogram of body weight. There is little variation in the blood volume of a healthy person over long periods, although each component of the blood is in a continuous state of flux. In particular, water rapidly moves in and out of the bloodstream, achieving a balance with the extravascular fluids (those outside the blood vessels) within minutes. The normal volume of blood provides such an adequate reserve that appreciable blood loss is well tolerated. Withdrawal of 500 millilitres (about a pint) of blood from normal blood donors is a harmless procedure. Blood volume is rapidly replaced after blood loss within hours, plasma volume is restored by movement of extravascular fluid into the circulation. Replacement of red cells is completed within several weeks. The vast area of capillary membrane, through which water passes freely, would permit instantaneous loss of the plasma from the circulation were it not for the plasma proteins—in particular, serum albumin. Capillary membranes are impermeable to serum albumin, the smallest in weight and highest in concentration of the plasma proteins. The osmotic effect of serum albumin retains fluid within the circulation, opposing the hydrostatic forces that tend to drive the fluid outward into the tissues.

The importance of potassium

Potassium is necessary for the normal functioning of all cells. It regulates the heartbeat, ensures proper function of the muscles and nerves, and is vital for synthesizing protein and metabolizing carbohydrates.

Thousands of years ago, when humans roamed the earth gathering and hunting, potassium was abundant in the diet, while sodium was scarce. The so-called Paleolithic diet delivered about 16 times more potassium than sodium. Today, most Americans get barely half of the recommended amount of potassium in their diets. The average American diet contains about twice as much sodium as potassium, because of the preponderance of salt hidden in processed or prepared foods, not to mention the dearth of potassium in those foods. This imbalance, which is at odds with how humans evolved, is thought to be a major contributor to high blood pressure, which affects one in three American adults.

The adequate intake recommendation for potassium is 4,700 mg. Bananas are often touted as a good source of potassium, but other fruits (such as apricots, prunes, and orange juice) and vegetables (such as squash and potatoes) also contain this often-neglected nutrient.

The effect of potassium on high blood pressure

Diets that emphasize greater potassium intake can help keep blood pressure in a healthy range, compared with potassium-poor diets. The DASH trial (Dietary Approaches to Stop Hypertension) compared three regimens. The standard diet, approximating what many Americans eat, contained an average of 3.5 daily servings of fruits and vegetables, which provided 1,700 mg of potassium per day. There were two comparison diets: a fruit- and vegetable-rich diet that included an average of 8.5 daily servings of fruits and vegetables, providing 4,100 mg of potassium per day, and a "combination" diet that included the same 8.5 servings of fruits and vegetables plus low-fat dairy products and reduced sugar and red meat. In people with normal blood pressure, the fruit- and vegetable-rich diet lowered blood pressure by 2.8 mm Hg (in the systolic reading) and 1.1 mm Hg (in the diastolic reading) more than the standard diet. The combination diet lowered blood pressure by 5.5 mm Hg and 3.0 mm Hg more than the standard diet. In people with high blood pressure, the combination diet reduced blood pressure even more, by as much as 11 mm Hg in systolic blood pressure and 5.5 mm Hg in diastolic pressure.

Potassium and stroke risk

High blood pressure is a leading risk factor for strokes, so it's no surprise that higher potassium is also associated with a lower stroke incidence. One prospective study that followed more than 43,000 men for eight years found that men who consumed the highest amounts of dietary potassium (a median of 4,300 mg per day) were 38% less likely to have a stroke as those whose median intake was just 2,400 mg per day. However, a similar prospective study that followed more than 85,000 women for 14 years found a more modest association between potassium intake and the risk of strokes. Additional research has mostly upheld these findings, with the strongest evidence to support high dietary potassium seen in people with high blood pressure and in blacks, who are more prone to high blood pressure than whites.


  • Try to eat more produce. Higher potassium consumption from foods, especially fruits and vegetables, may lower blood pressure and the risk of heart disease and strokes.
  • Never take potassium supplements without a doctor's prescription, as this can easily cause high blood potassium levels that are dangerous.
  • Pay attention to the potassium content of salt substitutes, since it can be high.

To learn more about the vitamins and minerals you need to stay healthy, read Making Sense of Vitamins and Minerals, a Special Health Report from Harvard Medical School.

Watch the video: How young blood might help reverse aging. Yes, really. Tony Wyss-Coray (January 2022).