Tailoring Exercise to Your Age

Len Canter wrote . . . . . . . . .

Exercise is a great way to stay youthful and even turn back the clock on aging. If you’re new to exercise or simply want a fitness reboot, here are ideas by the decade.

In Your 20s: Experiment with different workouts to find what you enjoy. Make exercise a regular habit that you won’t want to give up, even when career and family make heavy demands on you.

In Your 30s: Short on time? Try three 15-minute walks spread throughout the day. To stay fit and retain muscle, do cardio just about every day and strength training two or three times a week. If you’re new to exercise, take classes or have a personal trainer create a program for you.

In Your 40s: Enhance your weekly routine by doing both low-intensity exercise, like yoga for stress relief and flexibility, and high-intensity workouts, like interval training or a spin or kettlebell class, to boost calorie burn and muscle elasticity. Expect longer recovery times after high-intensity workouts, so make sure to get enough sleep.

In Your 50s: Regular exercise remains a must, but ask your doctor for modifications if you have any chronic conditions. Varying your workouts or taking up a new sport will engage your brain as well as different muscles. Get in at least one or two high-intensity workouts a week and try to take active vacations that include favorite pastimes like biking, hiking or even walking tours.

In Your 60s and Beyond: Stay fit and strong to stay independent longer, and stay socially engaged by taking group classes. Stick with strength training, but consider using machines rather than free weights for more control. Water workouts may be easier on joints, too, especially if you have arthritis. But always keep moving. Try tai chi for flexibility and balance, and go dancing for fun and fitness.

Source: HealthDay

Salmon and Dill Fishcakes


600 g potatoes, peeled and cut into chunks
3-4 tbsp vegetable oil
400 g skinned salmon fillet (in one piece)
200 g smoked salmon, chopped
1 tsp mustard powder
1 tsp horseradish sauce
zest of 1 lemon
small bunch of dill, fronds chopped
1 large egg, beaten
60 g fresh breadcrumbs
1/2 tsp celery salt
salt and pepper
lemon slices, to serve


  1. Cook the potatoes in a large pan of boiling salted water until soft but not completely falling apart (about 20 minutes). Drain and leave to steam dry in the colander. Mash well, using a potato ricer if you have one. Set aside.
  2. Heat 1 tablespoon of oil in a large frying pan and cook the salmon fillet over a medium heat for about 5 minutes each side. Transfer to a plate to cool.
  3. Flake the cooled salmon into a large bowl, feeling for any stray bones as you go. Add the mashed potato, smoked salmon, mustard powder, horseradish, lemon zest and beaten egg. Add most of the dill, saving a few fronds for garnishing at the end. Season with salt and pepper and then mix really well with your hands. Cover with cling film and chill in the fridge for at least 1 hour.
  4. When ready to cook, preheat the oven to 200ºC. Drizzle a tablespoon of oil over the base of a large baking tray.
  5. Mix together the breadcrumbs and celery salt in a shallow dish. Shape the chilled mixture into patties – you should get between 10 and 12 fishcakes. Press lightly into the breadcrumbs to coat all over and place on the baking tray.
  6. Drizzle the tops of the fishcakes with a little more oil and then bake in the oven for approximately 25 minutes, turning halfway through cooking. The fishcakes can also be pan-fried in a few tablespoons of oil over a medium heat. They will need about 6 minutes on each side.
  7. Sprinkle over the remaining dill and serve with the lemon slices.

Makes 3 to 4 servings.

Source: My Family Kitchen

In Pictures: Fish and Chip in the Restaurants of London, U.K.

Nutrition and Immunity

Ranjit Kumar Chandra wrote . . . . . . . . .


It is now generally accepted that nutrition is an important determinant of immune responses. Epidemiologic and clinical data suggest that nutritional deficiencies alter immunocompetence and increase the risk of infection. Poor sanitation and personal hygiene. overcrowding. contaminated food and water, and inadequate nutrition knowledge contribute to this susceptibility. Work done in the past 25 y has confirmed that impaired immunity is a critical adjunct factor in malnutrition-associated infection. This concept applies not only to young children in developing countries but also to all age groups in all populations of the world. including the elderly, those with eating disorders, and patients with a variety of primary debilitating diseases. A list of reviews and monographs is provided for further reading and citations to specific findings.

The Immune System

Detailed descriptions of the immune system and its dysfunction in primary and secondary immunodeficiency disorders can be found elsewhere. Host resistance mechanisms can be divided into two main tiers: nonspecific and antigen specific. The nonspecific defenses include the skin and mucous membranes, phagocytic cells, mucus, cilia, complement, lysozyme, interferon, and other humoral factors.

These innate processes are naturally present and are not influenced by prior contact with the infectious agent. They act as the first line of protection and retard the establishment of overt infection. Antigen-specific mechanisms include the B cell system of antibody production and the T cell system of cellmediated immunity. These mechanisms are adaptive and ac- quired in that they are specific reactions induced by prior exposure to the microorganism on its antigenic determinants.

They are effective in checking the spread of infection and eradicating the invading organism. The specific immune re- sponses form the basis of prophylactic immunization against common communicable diseases such as measles, respiratory illness caused by Hemophilus influenza, and systemic disease caused by Salmonella. In the body, nonspecific and antigenspecific defenses act in concert.

Protein-energy Malnutrition

Lymphoid atrophy is a dramatic feature of protein-energy malnutrition (PEM). The size and weight of the thymus are reduced. Histologically, there is a loss of corticomedullary differentiation; there are fewer lymphoid cells; and the Hassall bodies are enlarged, degenerated, and occasionally calcified. These changes are easily differentiated from findings in primany immunity deficiency, such as DiGeorge syndrome.

In PEM there is also a loss of lymphoid cells around small blood vessels in the spleen and in lymph nodes the thymusdependent paracortical areas show depletion of lymphocytes.

In PEM most host-defense mechanisms are impaired. Delayed-hypersensitivity cutaneous responses both to recall and new antigens are markedly depressed. It is not uncommon to have complete anergy to a battery of different antigens. These changes are observed in moderate deficiencies as well. The skin reactions are restored after appropriate nutritional therapy for several weeks or months. There is also a reduction in mature, fully differentiated T lymphocytes due in part to a reduction in serum thymic factor activity. Additionally, deoxynucleotidyl transferase activity in leukocytes is increased.

The proportion of helper inducer T lymphocytes recognized by the presence of CD4+ antigen on the cell surface is markedly decreased. There is also a moderate reduction in the number of suppressor cytotoxic CD8+ cells. Thus, the ratio of CD4+ to CD8+ cells is significantly lower than that in well- nourished control subjects. Moreover, co-culture experiments showed a reduction in the tiumber of antibody-producing cells and in the amount of immunoglobulin secreted. This may largely be due to decreased help provided by T lymphocytes. Lymphocyte proliferation and DNA synthesis are shown to be reduced, especially when the autologous plasma from a patient is used in cell cultures. This may he the result of inhibitory factors as well as deficiency of essential nutrients in the patient’s plasma.

Serum antibody responses are generally intact in PEM, particularly when antigens in adjuvant are administered or for materials that do not evoke T cell response. Antibody affinity, may provide an explanation for a higher frequency of antigenantibody complexes found in such patients. Secretory immunoglohulin A (sIgA) antibody concentrations are lower after immunization with viral vaccines; there is a selective reduction in sIgA concentrations with some compensatory increase in IgM concentrations in secretions. This may have several clinical implications, including an increased frequency of septicemia commonly observed in undernourished children.

Phagocytosis is also affected in PEM. Complement is an essential opsonin and the concentrations and activity of most complement components are decreased. The best documented is a reduction in C3, CS, factor B, and total hemolytic activity.

There is a slight reduction in opsonic activity of plasma. Furthermore, metabolic activation and intracellular destruction of bacteria are reduced. Finally. recent work in humans and animals showed that the production of several cytokines, including ititerleukins 1 and 2 and interferon y. is decreased in PEM. Moreover, malnutrition alters the ability of T lymphocytes to respond appropriately to cytokines. There is little work on the effect of malnutrition on the integrity of physical barriers, quality of mucus, or several other innate immune defenses. For example, lysozynie concentrations are decreased, largely as the result of reduced production by monocytes and neutrophils and increased excretion in urine. Adherence of bacteria to epithelial cells is an essential first step before invasion and infection can occur. The number of bacteria adhering to respiratory epithelial cells is increased in PEM.


Several trace elements and vitamins have an essential role in key metabolic pathways and immune cell functions. Isolated deficiencies of micronutrients are rare with the exception of iron, vitamin A, and zinc. However, they frequently complicate PEM and iiiany systemic diseases. Moreover, human malnutrition is usually a composite syndrome of multiple nutrient deficiencies.

Observations in laboratory animals deprived of one dietary dcnient and findings in the rare patient with a single nutrient deficiency have confirnied the crucial role of several vitamins and trace elements in immunocompetence. Detailed description of the effect of micronutrients on immune responses is given elsewhere.

Five general concepts have been advanced. First, alterations in immune responses occur early in the course of reduction in micronutrient intake. Second, the extent of immunologic impairment depends on the type of nutrient involved, its interactions with other essential nutrients, the severity of deficiency, the presence of concomitant infection, and the age of the subject. Third, immunologic abnormalities predict outcome, particularly the risk of infection and mortality. Fourth, for many micronutrients excessive intake is associated with impaired immune responses and, finally, tests of immunocompetence are useful in titration of physiologic needs and in assessment of safe lower and upper limits of micronutrient intake.

Zinc is chosen as an example to illustrate these concepts. Zinc deficiency, both acquired and inherited, is associated with lymphoid atrophy, decreased delayed-hypersensitivity cutaneous responses, delayed homograft rejection, and lower thymic hormone activity. Patients with acrodermatitis enteropathica have impaired lymphocyte response to phytohemagglutinin, decreased thymulin activity, and reduced delayed-hypersensitivity cutaneous reactions. In laboratory animal models these findings can be confirnied and, in addition, one can show a reduced number of antibody-forming cells in the spleen and impaired activity of T killer cells, decreased ingestion, and reduced phagocytosis. Zinc is probably involved in stimulation of NADPH oxidase through its role as a cofactor for phospholipase A2 or phospholipase C. Zinc may stabilize arachidonic acid against oxidation by iron complexes. Zinc complexes may react with oxygen, generating products highly toxic to ingested pathogens. Wound healing is impaired in zinc deficiency. Zinc deficiency increases morbidity and mortality of animals challenged wtth various organisms, including Enterovirus coxsackie B and Lisieria monocytogenes. Zinc deficiency promotes the establishment of nematodes and alters the characteristics of their expulsion from the intestine although spontaneous cure is unaffected.

Important work needs to he done on the molecular basis of impaired lymphocyte and phagocyte functions in zinc deficiency. A slight excess intake of certain nutrients such as zinc may he associated with enhanced immune responses. It is known now that almost all nutrients given in quantities beyond a certain threshold will reduce immune responses. This has been shown for zinc for both phagocyte and lymphocyte functions. The mechanisms of these immunotoxic effects are not clear, but for zinc overdose, alterations in serum and cell-bound low-density lipoproteins reduced concentrations of other nutrients; changes in membrane structure and receptor expression are some possibilities.

The Elderly

There is much recent interest in and work on the effects of dietary intake and nutritional status on immunity and risk of illness in old age. The pattern of illness observed in the elderly suggests that immune responses decline in old age. Because of the close contact of the immune system with other systems in the body, any changes in immunocompetence can be expected to influence other organ functions as well. As immunologic vigor declines, incidences of infections, cancer, immune complex disease, autoimmune disorders, and amyloidosis increase.

Cellular and molecular manipulation including nutritional support to prevent or slow the decline of immune functions can be expected to delay the onset or decrease the severity of pathology associated with aging.

Age-related changes in immune responses have been the focus of much recent work. The number of plunipotent cells with the ability to colonize peripheral lymphoid sites and to mature into competent cells decreases with age. The ability of stem cells to undergo clonal proliferation decreases and the generation of B cells and homing of precursor cells into the thymus is reduced. This restraint on stem cell kinetics and reserves may be critical to an effective response to stress, such as infection.

Elderly patients with sepsis often fail to mount leukocytosis, although the expected shift to the left of immature polymorphonuclear leukocytes does occur. In the elderly, delayed-hypersensitivity cutaneous responses to ubiquitous recall antigens derived from bacterial and fungal products, as well as to 2,4-dinitrochlorobenzene, are reduced in frequency and in size. Lymphopenia and anergy have important prognostic significance in old age. The number of circulating T lymphocytes is slightly decreased. The number of CD4+ cells is decreased, whereas the number of CDS+ cells is variously reported as normal, decreased, or increased. Functional alterations associated with these changes in the number of cells include decreased lymphocyte proliferation in response to mitogens and antigens, reduced production of macrophage migration inhibition factor and of interleukin 2, impaired mixed lymphocyte reaction, and decreased natural killer cell activity. There is also a sharp decline in thymulin activity.

There is a reduction in serum IgG concentration and an increase in serum IgA. Generally, primary antibody response is decreased but antibody titer after booster immunization is often comparable in the young and the elderly. There is, however, a delay in reaching the peak antibody response in the elderly.

For many antigens, antibody production by B cells requires helper factors generated by T cells. Antibody responses to such antigens are decreased in old age and the affinity of the antibody may be reduced. There are no data on sIgA antibody responses of old individuals. Polymorphonuclear leukocytes obtained from the elderly have reduced migration ability, both random and chemotactic. The uptake of microorganisms is slightly reduced and has been attributed to a more rigid cell membrane. There is partial reduction in the magnitude of the metabolic burst associated with phagocytosis, and lysis of Candida is impaired.

Nutritional deficiencies are seen in at least one-third of the elderly in industrialized countries. Certain old individuals are at particularly high risk of malnutrition: the physically isolated; those living alone, especially those who have been recently bereaved; the socially isolated; those with sensory on mental impairment; those with a chronic systemic disease; the very poor; and the very old. Furthermore, a reduction in total energy intake results in inadequate consumption of certain essential nutrients. This is further compounded by a lack of variety and characteristic self-selection of food items, the presence of malabsorption in some elderly individuals, and drug-nutrient interactions.

The simultaneous assessment of nutritional status and immune responses and subsequent correlation analysis have suggested that impaired immunity in the elderly may be due in part to associated nutritional deficiencies. Several recent studies attempted to correct nutritional deficiencies in the elderly and examined the effects of such interventions on immune responses. In general, providing extra energy or multiple micronutnients or moderately large doses of single nutrients resulted in improved immune responses. In a few studies, this was associated with reduced infection-related illness. Much more work needs to be done in this area of considerable public health significance.

Concluding Remarks

The well-established effect of nutrition on immunity has led to several practical applications. These include the use of immunologic tests as prognostic indexes in patients undergoing surgery and the use of immunologic methods to assess nutnitional status and to judge the adequacy of nutritional therapy and improved immunologic response to and protective efficacy of vaccines. Finally, this new knowledge has permitted the development of designer feeding formulas with selective ingredients in specified amounts: these feeding formulas have been shown to reduce the risk of infection in animal models and in immunocompromised hosts. Clearly, the work on nutrition and immunity reviewed here has had a significant and crucial influence on public health and clinical medicine.

Source: Watermark

Exercise to Strengthen the Immune System

We have often seen studies on how various forms of exercise help maintain bone density, increase muscle mass, reduce fat, improve heart and lung function, reduce stress, heighten moods, and so on. But today we are focusing on what exercise does for the immune system.

Getting the body moving on a moderate level, promoting blood flow, deepening breathing, and increasing range of motion in our joints, work to stimulate the immune system. For the sake of this discussion, “moderate exercise” can be defined as walking, yoga or Tai Chi, riding a bike on level ground, or swimming. The idea is to get moving at a level that is comfortable to you that will increase your breathing and blood flow.

The increase in blood circulation helps white blood cells and antibodies quickly respond to identified invaders in your body. These unwanted invaders include viruses and bacteria. By increasing the response time for your body’s defenses, you are improving the chance of neutralizing the culprits before they can multiply and establish a fortified defense against you.

One of the workhorses in your immune system is a group of white blood cells known as lymphocytes, which include B-cells and T-cells. Both of these cell-types are instrumental in protecting you from germs and toxins. The key interaction between B- and T-cells, and “invaders”, occurs in your lymph glands, and an activator of your lymphatic system is deep breathing. Further, the movement of your arms and legs provide a pumping action that help stimulate the circulation of lymph fluid throughout your system.

This time of year is often accompanied by stressors that can mess with our heads; anxiety, depression, moodiness, etc. It is always amazing how a little activity seems to decompress the mind, and lift the spirit, with something as simple as going for a walk.

Oxygen also plays a role in improving your immune system. Starting way back in 1931 (when Otto Warburg was awarded his Nobel Prize for research on the link between cancer and adequate oxygen to the cells), there has been a growing body of evidence indicating the link between immune deficiency and reduced oxygen metabolism.

The main theme of this discussion is that it benefits us to simply get moving. However, it should be noted that — like many instances where too much of a good thing can be bad — too much exercise will actually suppress the immune system. Folks who are serious about intense athletic endeavors can find themselves “over-trained”, feeling lethargic and susceptible to every cold the kids bring home. For those of us who partake in the higher demands of intense activities, a dedicated routine of exaggerated levels of antioxidant supplementation and disciplined rest periods are vital for staying on our feet.

One more aspect of moderate exercise is the mental connection. Holiday events, extended weekends, and even family vacations are often accompanied by stressors that can mess with our heads; anxiety, depression, moodiness, etc. It is always amazing how a little activity seems to decompress the mind, and lift the spirit, with something as simple as going for a walk.

So, the next time the “good times” begin to press you down, get up and move… and I don’t mean to Miami. I mean simply stand up and start moving. It’s good for you.

Source: Applied Health

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