In traditional Chinese medicine, bone health is believed to be inextricably linked to the health of the kidneys. So any treatment recommended for strengthening the kidneys (increasing their “energy”) would be good for your bones as well. The kidneys are also thought to be related to aging in general. Chinese medicine has long been used to relieve the symptoms of a difficult menopause with much success, so low bone density might also be improved along with more overt signs of a drop in hormone levels.
An expert in Chinese medicine will generally recommend a combination of diet, herbs, acupuncture, and exercise, particularly tai chi and qi gong, or a similar type of movement. I’m a fan of this kind of exercise, as described earlier in the book, since it builds bone mass and develops strength and balance, and at the same time reduces stress, so that’s one of the appeals of TCM to me. Acupuncture has some of the best science behind it of any other “alternative” therapy. But the key thing about traditional Chinese medicine is that it uses a combination of tactics that are greater than the sum of their parts. You can use just one strand, if necessary, but weaving them together results in a stronger whole cloth.
Acupuncture is an excellent way to relieve pain, including pain from osteoporosis or low bone density. The Kidney 3, Kidney 10, and Spleen 6 points for acupuncture—or acupressure, if you want to try this at home—are important for preventing and treating low bone density and the pain that can result. (If you don’t get results with self-administered acupressure, don’t throw the baby out with the bathwater. Working with a properly trained acupuncture professional could well make all the difference.) If done properly, it can also alter the body’s metabolism and biochemistry in ways Western science does not yet fully understand to actually stimulate bone growth and retard loss. It is generally acknowledged that acupuncture points have more nerves and increased blood flow than the areas around them, so stimulating them produces changes in nerve conduction and releases serotonin and endorphins, which improve mood and decrease pain throughout the body, among other things.
I read an anecdote in an alternative medicine reference book from a leader of a school of traditional Chinese medicine who treated a woman whose bone density was 30 percent below desirable. After two and a half months of acupuncture and herbs (and no other intervention), she had no more pain and her bone density had increased 50 percent. Blood tests showed her hormone levels had Increased. The expert in traditional Chinese medicine I work with doesn’t have his clients get bone scans, but reports his patients with suspected low bone density find balance and strength with the practice of traditional medicine, with little in the way of menopausal complaints.
For a shot at such remarkable results, consult a specialist in Eastern medicine, not someone with just the few months’ training required to hang out a shingle. Only a few hundred people in this country have taken the four- to five-year formal medical training available to become experts, and the number of people with the less intense training is growing by leaps and bounds. (A good acupuncturist should be able to help you with symptom relief, at least, even with the more rapid training course.)
Chinese herbs are usually given in combination and treat your body’s unique energy. So again you should seek professional guidance to find the mix that is best for you. Good herbologists won’t give generic recommendations for particular conditions. Rather, they treat each individual by working to restore balance to the body overall. If you want to experiment yourself, eycinnuam dipsaci is a common recommendation. Dong quai contains phytoestrogens 1/400 as strong as estrogen, but with some of the same effects on the body. (Do not take dong quai if you are pregnant.) Two Immortals Decoction and Eight Flavor Rehmannia formulas are generally good choices for women looking to protect their bones. Six Flavor Rehmannia supports the kidney, as do shou wu, dong quai, and ginseng, which are often used in combination (including a drink called Shou Wu Chih) for easing the aging process. Ginseng has a lot of beneficial phytoestrogens, but use it carefully, as high levels can cause high blood pressure, anxiety, and insomnia. Ox knee root and three-edge root have estrogenic effects, which should support healthy bones. In an animal study, tochu bark extract was proven to help the body absorb calcium, and was shown to increase bone density and muscle mass. In humans, licorice (gan cao) and peony (bau shao and chi shao) have been shown to increase the ratio of estrogen to testosterone, following animal studies that revealed the herbs helped convert testosterone into estrogen, raising overall estrogen levels. Liu wei di huang tang formula can increase estrogen levels and estrogen receptors after menopause. Dan shen also increased estrogen levels in another study in animals.
Be aware that using these herbs off-the-rack, without consulting with an expert, isn’t really traditional Chinese medicine (though it may or may not work for you). Simply substituting another chemical (“natural” though they may be, herbs work because they are sources of potent chemicals) for a prescription won’t get you any closer to optimal health or bone density.
*166\228\2*

You’re playing basketball, you come down from a rebound, and suddenly you’re in terrible pain. Your knee swells up, and you can’t straighten your leg. This is the typical scenario of a patellar tendon rupture, an injury that most often affects people in their forties while they are engaging in physical activity, although in more rare cases, it could also be caused by another type of injury, such as a fall.
In some cases, the tendon may only be partially ruptured, which is painful but not as serious as a complete rupture.
Diagnosis
Similar to a quadriceps tendon rupture, patients with a patellar tendon rupture will not be able to straighten their injured leg. In addition, they will be in a great deal of pain.
On an X ray, the patella will appear in a somewhat higher position (a few millimeters higher) on the knee than normal.
An MRI can determine if the rupture is complete or partial.
Treatment
A complete rupture must be surgically repaired with open-knee surgery. The tendon ends must be cleaned, reattached, and sutured back to the patella or tibia, depending on the location of the tear. You will then be casted for anywhere from 3 to 6 weeks, and once the cast is removed, you will begin exercises to restore your full range of motion. Leg strengthening exercises are also essential to help build up strength in the injured leg so that it is equal to the noninjured leg.
*44\185\2*

Although pregnancy might affect your seizures, your risks during pregnancy are little different from the risks other women face. If you have questions about conditions that might have caused your epilepsy or about the effect of pregnancy on other health problems, you should check with your physician before you decide to become pregnant.
Your seizures may change during pregnancy. Therefore, your obstetrician needs to know about your epilepsy and your neurologist about your pregnancy. In about one-third of pregnant women, seizures get worse, in one-third they improve, and in one-third they are unchanged. Since we cannot predict which group you will fall into, your pregnancy should be monitored carefully. Ideally you should be on the lowest amount of a drug, and on a single drug only, to control your seizures. This drug, and its level, should, if possible, be determined before you become pregnant. Anticonvulsants should not be changed during your pregnancy unless such a change is needed for seizure control or because of toxicity.
Since blood levels change as your body chemistry itself changes during the pregnancy, blood levels of your medications should be monitored. We generally recommend that these levels should be measured early in the pregnancy, then followed every month in the middle third of your pregnancy and every several weeks in the last trimester.
There are three principal reasons why seizures increase during pregnancy in almost one of three women with epilepsy. The first is that pregnant women are naturally fearful that taking drugs may affect the fetus and, therefore, may fail to take anticonvulsant medication according to schedule. A second reason is lack of sleep during pregnancy. A third cause of seizures during pregnancy is changes in the body’s metabolism of drugs. Although such changes can cause blood levels to rise and thus cause toxicity, blood levels can also decline, leading to seizures. Your physician should closely follow your blood levels and provide appropriate adjustments.
Although there is little evidence that brief seizures injure the fetus, a prolonged seizure might affect your fetus and any seizures might cause injury to you. Therefore, we strongly urge that pregnant women with epilepsy who need medication for seizure control continue to take the drug that has been controlling their seizures.
*266\208\8*

Individuals who have epilepsy controlled with medication and whose physicians are now recommending discontinuing medication pose special dilemmas for both the physician and the driver. Optimally, we would like to help patients be free of medication if possible. While in an ideal patient the risk of recurrent seizures is small, if they recur it is most likely to happen in the first three to six months after stopping medication. Most physicians recommend that the patient should not drive during that period of increased risk. If driving is absolutely essential, then risks should be minimized by limiting the amount of time behind the wheel. Driving while tired or for long distances should be avoided during this period.
Clearly there is need for better information on the risks of driving with epilepsy. Such information should assess the risks of recurrence of seizures and factors which are predictive of such a recurrence, as well as the risks and hazards of accidents and of injuries to others. These risks should be placed in the perspective of other health-related disabilities. The driving risks represented by persons who use drugs and alcohol far outweigh the risks associated with epilepsy. These factors should be considered by the regulating agency when deciding whose driving should be restricted and for how long. The availability of restricted licenses that might permit an individual to drive to work or to school or only under certain restricted circumstances might balance the public’s risk of allowing some people with epilepsy to drive against the high cost of restricting the privilege.
Above all, decisions about driving need to be based on individual needs and capacities.
*263\208\8*

A. Tumor lysis syndrome
1. Overview
a. Acute tumor lysis syndrome is a consequence of the rapid release of intracellular metabolites (uric acid, potassium, and phosphorus) in quantities that exceed the excretory capacity of the kidneys.
b. Renal failure and hypocalcemia are common complications.
2. Etiology
a. Tumor lysis syndrome is seen in tumors that have a high growth fraction and that are exquisitely sensitive to chemotherapy.
b. Burkitt lymphoma and T-cell leukemia-lymphoma syndrome and/or hyperleukocytosis are the most common causes. Evidence for the onset of tumor lysis can be found before beginning therapy, because of sponta-eous tumor degradation, and also from 1 to 5 days after the initiation of treatment.
3. Evaluation
a. Perform repeated physical examinations.
b. Measure urine output, blood pressure, and weight 1-3 times daily.
c. Monitor serum creatinine, uric acid, calcium, sodium, phosphate, and potassium every 8 hours until the risk period is over.
d. If the patient remains oliguric, imaging studies of the kidney may be useful to rule out obstructive uropathy.
4. Prevention
a. Urine output should be maintained at >5 mL/kg/h before initiating chemotherapy and at >3 mL/kg/h once chemotherapy is begun, and verified every 2 to 4 hours. If urine output falls, institute corrective measures promptly (more fluids and/or diuretics).
b. Assure adequate hydration by replacing calculated deficits: intravenous (IV) fluids at 3000 mL/m2/day; may need to increase fluids further to maintain urine output.
c. Diuresis with furosemide (Lasix) (0.5-1 mg/kg) or mannitol (circulating fluid volume must be adequate: 5-15 g/m2 as 2596 solution over 5-10 minutes repeated every
6 hours as necessary to achieve desired urine volume).
5. Management
a. Hyperuricemia (>8 mg/dL)
An elevated uric acid results from nucleic acid breakdown. Urates can precipitate in the acid environment of the kidney, causing renal failure.
i. Allopurinol 300 mg/m2/day divided t.i.d.
ii. Alkalinization of urine pH from >6.5 to <7.5 with NaHC03 120 mEq/m2/day IV will increase the solubility of urates; pH >7.5 is associated with a precipitation of hypoxanthine as well as calcium phosphate crystals. Alkalinization should be discontinued once uric acid is controlled and/or if phosphorus is elevated.
b. Hyperphosphatemia (>6.5 mg/dL)
Lymphoblasts have four times the content of phosphate of normal lymphocytes. When the calcium phosphate product exceeds 60, calcium phosphate precipitates in microvasculature and renal tubules, which can lead to renal failure.
i. Low-phosphate diet
ii. Aluminum hydroxide 150 mg/kg/day divided q4-6h
iii. urine output >3 mL/kg/h
c. Hyperkalemia (>6.0 mEq/L)
Potassium can be elevated because of tumor lysis or secondary to renal failure. Hyperkalemia leads to ventricular arrhythmias and death.
i. Do not administer intravenous potassium until the
tumor lysis is controlled.
ii. Sodium polystyrene sulfonate (Kayexalate) removes 1 mEq potassium/L/g resin over 24 hours; give as 1 g/kg PO q6h with sorbitol 50-150 mL. This is not an emergency intervention. The duration of action depends on the rate of endogenous potassium release.
iii. Administering calcium is the fastest means of reversing the cardiac effects of hyperkalemia. The onset of action is within minutes, but the duration of action is only about a 1/2 hour. Administer for life-threatening arrhythmias as calcium chloride 10 mg/kg IV. (Do not administer in the same line as sodium bicarbonate.)
iv. Sodium bicarbonate at 1-2 mEq/kg IV will drive potassium into the cell. For every increase in 0.1 pH unit, potassium decreases about 1 mEq/L. The onset of action is in 1/2 hour; the duration of activity is several hours.
v. Administering insulin and glucose will also move excess potassium into the cell. Glucose is administered continuously at 0.5 g/kg/h with insulin 0.1 U/kg/h. Monitor serum glucose closely and adjust infusion rates appropriately. In an emergency, glucose alone can facilitate potassium entry into the cell (1 mL/kg of 5056 dextrose in a central line). Onset is in 20-30 minutes; the duration of activity is several hours.
d. Hypocalcemia (ionized calcium <1.5 mEq/L) Hypocalcemia occurs secondary to hyperphosphatemia as a compensatory mechanism to maintain the calcium phosphate product at 60. i. For symptomatic hypocalcemia, administer 10 mg/kg of elemental CaCl in a drip over several minutes. ii. Discontinue administration when symptoms resolve. e. Dialysis Indications include fluid overload with congestive heart failure, anuria, symptomatic hypocalcemia with hyperphosphatemia, hyperkalemia with QRS interval widening which generally occurs with potassium >6, and elevated creatinine with poor urine output.
f. Institute hyperleukocytosis interventions if appropriate.
B. Hypercalcemia
1. Overview
a. Hypercalcemia, a paraneoplastic syndrome, although rarer in children than in adults, has been reported in patients with leukemias, lymphomas, rhabdomyosarcoma, neuroblastoma, Ewing sarcoma, Wilms tumor, and rhabdoid tumors of the kidney.
b. Mechanisms postulated to be the cause for the hypercalcemia are the following.
i. Production by the tumor of a parathyroid hormone-related protein
ii. Production by the tumor of bone-resorbing substances (Iymphotoxin and tumor necrosis factor)
iii. Elevation of 1,25 dihydroxyvitamin D
iv. Production of parathyroid hormone
c. All the above cause excess release of calcium from bone into the blood. This results in polyuria, dehydration leading to diminished glomerular filtration with increased renal absorption of calcium, worsening the hypercalcemia.
2. Evaluation
a. The normal value of calcium corrected for albumin is 9-11 mg/dL (4.5-5.5 mEq/L). Mild hypercalcemia can be defined as 12-14 mg/dL (6-7 mEq/L) and severe hypercalcemia is >15 mg/dL (7.5 mEq/L). Add 0.8 mg/dL of calcium for every gram per liter reduction of serum albumen.
b. Non-protein-bound ionized calcium (normal = 1.00-1.31 mmol/L) is of greater physiologic importance and does not need correction for serum protein.
Management
a. Mild hypercalcemia
i. Administer intravenous hydration with normal saline (3000 mL/m2/day) and encourage oral intake. High fluid volume promotes the excretion of calcium, and saline interferes with the reabsorption of calcium in the proximal tubule of the kidney.
ii. Furosemide 1-2 mg/kg IV t.i.d. or q.i.d. blocks the
reabsorption of calcium in the ascending loop of
Henle.
iii. Monitor electrolytes frequently.
iv. Maintain exercise and movement.
b. Severe hypercalcemia
i. Increase intravenous hydration to 6000 mL/m2/day and continue furosemide as above.
ii. Administer biphosphonates such as pamidronate 60 mg IV over 4 hours once for children over 50 kg. May repeat in 7 days as necessary The dosage for smaller children has not been established. Action results in an inhibition of bone resorbtion.
iii. For lymphoproliferative disorders, steroids (prednisone 2 mg/kg/day or its equivalent) may decrease serum calcium over several days of use.
iv. Calcitonin, gallium nitrate, indomethacin, and mithramycin have all been used with some success but should be tried only if the above fails.
v. Oral or intravenous phosphates seem to have more toxicity than benefit. They decrease bone resorption and can increase extraosseous bone formation, possibly leading to increased renal toxicity. If they are used, monitor carefully, vi. For patients refractory or resistant to other methods of treatment, dialysis, either peritoneal or hemodialysis, can be used.
C. Syndrome of inappropriate antidiuretic hormone
1. Overview
Antidiuretic hormone (ADH or arginine vasopressin) causes the resorption of free water at the renal collecting duct; thus, it is an important mechanism in regulating the volume and osmolality of extracellular fluid.
a. ADH is released from the pituitary gland when osmoreceptors in the hypothalamus detect increased osmolality of the serum.
b. Secretion of ADH also occurs when volume receptors in the left atrium, carotid sinus, and aortic arch detect decreased effective circulating volume.
c. Volume depletion stimulates the secretion of ADH regardless of serum osmolality.
2. Etiology
The syndrome of inappropriate antidiuretic hormone (SIADH) exists when the release of ADH occurs in the absence of increased serum osmolality or volume depletion and is not suppressed by further volume depletion. It may occur with the following.
a. Malignancies (e.g., leukemia, lymphoma, Ewing sarcoma, and brain tumor)
b. Drugs (e.g., vincristine, vinblastine, barbiturates, and opiates)
Cyclophosphamide produces a SIADH-Iike syndrome by acting directly at the kidney tubule to enhance the absorption of free water.
c. Head trauma
d. Infection of the central nervous system (CNS) or lungs
e. Pain and/or stress
f. Surgery
3. Evaluation
a. The urine is maximally dilute with a relatively high urinary sodium (>20 mEq/L) despite hyponatremia and low serum osmolality.
b. Volume depletion, nephrotic syndrome, adrenal insufficiency, hypothyroidism, and congestive heart failure are absent.
4. Management
a. Treatment of the underlying disorder
b. Mild disease
i. Fluid restriction, equaling urine output
ii. Normal maintenance of Na+ intake
c. Severe hyponatremia (120-125 mEq/L) without life- threatening symptoms
i. Furosemide 1 mg/k promotes a free water diuresis.
ii. Replace urine loss milliliter for milliliter with normal saline.
iii. Demeclocycline 6.6-13.2 mg/kg divided into 2-4 doses (maximum 600-1200/day) inhibits the action of ADH on renal tubules by interfering with the formation and action of cyclic adenosine monophosphate.
d. Life-threatening neurologic symptoms (convulsions and stupor)
i. Furosemide 1 mg/kg promotes a free water diuresis.
ii. To correct sodium to 120 mEq/L, give 200 mL/m2 of 1.5% NaCl in 6-8 hours, and then more slowly to normal over 24-72 hours.
iii. It is important to avoid a rapid correction of serum sodium. Hypertonic sodium causes a sodium diuresis and may exacerbate the loss of sodium. Neurologic deterioration and death have occurred with too-rapid correction of serum Na+.
Hypokalemia
1. Overview
a. Normal serum potassium is 3.5-5.5 mEq/L; electrocardiogram (ECG) changes are seen at <2.5 mEq/L.
b. The principal effects are on cardiac rhythm, with symptoms occurring most commonly when the cause is acute.
c. Patients may develop ileus or muscle weakness.
2. Etiology
a. Renal wasting secondary to drugs is the usual etiology in pediatric cancer patients.
b. Commonly administered agents associated with tubular potassium loss include amphotericin B, antipseudo-monal penicillins, aminoglycosides, ifosfamide, cisplatin, loop diuretics, and glucocorticoids.
3. Evaluation
a. A semiquantitative assessment of potassium needs per day determines the potassium content of the patient’s spot urine and the 24-hour urine output.
b. Serum magnesium must be assessed, as potassium
cannot be conserved without adequate magnesium.
4. Management
a. Oral therapy is indicated for chronic hypokalemia.
b. Intravenous replacement is indicated for an acute decrease (particularly <2.5 mEq/L) or if the patient cannot take an oral supplement. c. The potassium infusion rate should not exceed 0.5 mEq/kg/h. d. Potassium concentrations of 100 mEq/L are acceptable in a central line. Concentrations > 40 mEq/L administered via peripheral vein are irritating or painful and can cause phlebitis.
e. ECG monitoring throughout IV potassium replacement is essential.
f. Potassium-sparing diuretics such as amiloride or
aldactone may help conserve potassium.
*58\168\2*

High amounts of daily protein cause a high incidence of carcinogenesis in animals. In many animal studies carcinogenesis was suppressed when animals were fed levels of protein that were at the minimum or below the minimum required for optimal growth.
There has been a fair amount of epidemiological human data to support that total protein intake will correlate with the incidence of and mortality from cancers of various sites. This correlation has been seen for breast cancer and colon and rectal cancer. There has also been a weaker association between high protein intake and other cancers, specifically pancreatic cancer, prostate cancer, and endometrial cancer.
Many of the studies included the consumption of fat as well as protein. Because there is not one but two variables, it is not possible to say with any certainty that high protein per se will be a factor in the cancers described.
The evidence linking pure sugars to the incidence of cancer is much weaker. A high dietary intake of refined sugar was one of the dietary components linked to the increased incidence of breast cancer in several studies.
To date, the evidence from both epidemiological and laboratory studies is too inconclusive to suggest any role for carbohydrates in carcinogenesis. But as we have already discussed, excessive carbohydrate ingestion contributes to obesity, which, in turn, has been implicated in carcinogenesis.
*57\360\2*

If you are using the 24-hour plan, and the 10-minutes-at-a-time plan for bad moments, you will get through somehow.
Sometimes the first few days are full of dreadful moments. You find you cannot work at anything. Your head is all over the place. You cannot sleep. You cannot relax. And yet you are horribly, appallingly exhausted all the time.
Naturally this means that you may not cope too well. You may find that very small set-backs such as missing a bus make you want to cry or rage. There may be difficulties at home or at work. None of these matter in the long run – as long as you do not use drugs or pick up a drink.
Whatever happens, whatever crises occur, whatever you do or don’t do, in the long run you are doing all right if you’re staying clean. Every day is a triumph for an addict who manages to stay away from drugs and for an alcoholic who stays sober.
So don’t put yourself down. Remember that even if the world seems to be falling apart around you, everything will come out right in the end – just as long as you manage to stay away from drugs or drink.
If you are staying clean and sober, you are in there with a good chance, no matter how terrible you feel. If you go back on the bottle or back to using drugs, then that chance has utterly vanished.

*88\116\2*

Withdrawal symptoms are extremely unpleasant. Indeed, this is often why people stay on drugs in the first place – to avoid withdrawal pain. Addicts are particularly bad at living through pain, because they have used their drugs to escape unpleasant reality.
Yet if you want to get well, you will have to learn to cope with the first few days of withdrawal. You have probably done it before. Thousands of recovering addicts have discovered the fundamental principles of coping with withdrawal. If they can do it, you can do it too.
1. A craving for the drug does not mean you have to take the drug. Live through the craving. It is possible to live through persistent, even continuous, craving for days or weeks. In the next chapter we will give you some mental tricks that will carry you through.
2. Live through the feelings of discomfort. Addicts who are using drugs are often very bad indeed at enduring pain, whether it is physical or emotional pain. They are used to blotting it out with drugs. So the trick of coming off drugs is to learn to live through the pain – literally to endure it. This is why it is important to keep busy going to NA or AA meetings in the first few weeks. It helps distract the mind from the pain. Comfort yourself with the thought of how this discomfort will last only a few days.
3. Talk about what you are going through. This is another reason for going to NA and AA meetings. The illness of chemical dependence can partially be talked out of the system in these meetings. Share your pain with others, and you will find that it has diminished in its intensity.
4. Withdrawal symptoms are a sign of recovery. This is the good news. The drug-using addict doesn’t suffer from withdrawal – only the recovering addict has these discomforts. They are the first signs of the body, mind and heart coming out of the illness. Keep remembering this. Remember too that there is a lot of happiness awaiting you.
5. You only have to do it once. You will never have to go through this withdrawal pain again, if you put your heart and soul into recovery. Unlike all the bad times on drugs, this bad time when you are getting clean and sober is a once-and-for-all experience.

*75\116\2*