What the JAK2 Test and Hematocrit Reveal Before Polycythemia Vera Treatment Starts

The routine blood count was supposed to be the boring part of the annual physical. Instead, a line on the printout came back flagged in red, the hematocrit sitting several points above the reference range, and a short note from the clinic: please book a follow-up and expect a second draw. A week later the phrase “JAK2 test polycythemia vera” is open in a browser tab at midnight, next to a half-finished search about whether this is cancer, whether it runs in families, and what a gene in the blood can possibly say about a number that sounds like a sports statistic.

That gap between the first abnormal result and the first real conversation with a hematologist is where most of the worry lives. It is also where the two tests in the title do their most useful work. One is a percentage; one is a genetic switch. Read together, they tell a surprisingly clear story.

This explainer walks through what each test measures, what the results mean, where they fall short, and how a care team turns them into a plan. No decision here belongs to a web page; every one belongs to the clinician holding the full chart.

What is polycythemia vera, in plain language?

Polycythemia vera, usually shortened to PV, is a slow-growing blood disorder in which the bone marrow makes too many red blood cells, and often too many white cells and platelets as well. It belongs to a family called myeloproliferative neoplasms: conditions in which a single marrow stem cell picks up a mutation and its descendants crowd out normal production. Because a mutated clone is driving the process, PV is classified as a chronic blood cancer, though it behaves very differently from the acute leukemias most people picture when they hear that word.

The practical problem is viscosity. Red cells carry oxygen, but pack too many of them into the same volume of plasma and blood flows like syrup rather than water. That sluggish flow is why the headline risk of PV is clotting: strokes, heart attacks, deep vein thrombosis and, less commonly, clots in the veins draining the liver or gut. Thicker blood also explains some of the day-to-day symptoms clinicians ask about, such as headaches, dizziness, blurred vision, itching after a warm shower, and a reddish flush to the face.

PV is uncommon. Most people are diagnosed around age 60, and it is slightly more frequent in men than in women, according to MedlinePlus Genetics. Many are picked up exactly the way the person in our opening scene was: through a routine blood count ordered for another reason, before any symptom has become obvious.

Two features make PV stand apart from the other causes of a high red cell count. First, the marrow is overproducing on its own, not in response to low oxygen or a hormone signal from elsewhere in the body. Second, in the overwhelming majority of cases, a specific mutation in the JAK2 gene can be found in the blood. That mutation is what the JAK2 test is looking for, and the hematocrit is the number that first raises the question.

Which blood test shows polycythemia? Start with the hematocrit

The hematocrit is the share of your blood volume that is made up of red cells, expressed as a percentage. A spun tube of blood separates into a pale plasma layer on top and a dense red column at the bottom; the hematocrit is simply how tall that red column is relative to the whole. Reference ranges vary by laboratory, but Mayo Clinic lists roughly 38.3 to 48.6 percent for adult men and 35.5 to 44.9 percent for adult women.

Hemoglobin, the oxygen-carrying protein inside red cells, is reported alongside it in grams per deciliter and tends to rise and fall in parallel. The World Health Organization criteria used to diagnose PV set the bar at a hemoglobin above 16.5 g/dL in men or 16 g/dL in women, or a hematocrit above 49 percent in men or 48 percent in women, as published in the 2016 revision of the WHO classification.

A single high reading, though, is a prompt rather than a verdict. Dehydration shrinks the plasma portion and makes the red cells look more concentrated than they really are; this is sometimes called relative or apparent polycythemia. Heavy smoking, untreated sleep apnea, lung disease, living at altitude, certain kidney tumors and testosterone therapy can all push the marrow to make more red cells for reasons that have nothing to do with a mutation. That is why a clinician usually repeats the count, checks the rest of the panel, and asks a few pointed questions before anyone says the words polycythemia vera.

Three other numbers on the same complete blood count matter more than people expect. A raised white cell count and a raised platelet count point toward a marrow that is overproducing across the board, which is typical of PV and unusual in secondary causes. A low erythropoietin level, measured on a separate test, points the same way. When those line up with a high hematocrit, the JAK2 test moves from optional to essential.

How the JAK2 test for polycythemia vera works

JAK2 stands for Janus kinase 2, an enzyme that sits just inside the surface of blood-forming cells and relays the message from erythropoietin, the kidney hormone that tells the marrow to make red cells. Think of it as the ignition switch. Normally it fires only when the hormone turns the key. The mutation most often found in PV, called V617F because it swaps one amino acid for another at position 617 of the protein, leaves the switch jammed in the on position. The marrow keeps producing whether or not the body needs more oxygen carriers.

The JAK2 test for polycythemia vera is a DNA test run on an ordinary blood sample, not a biopsy. The laboratory extracts DNA from white cells, then uses a polymerase chain reaction, a technique that copies a chosen stretch of DNA millions of times, to look for the altered sequence. Because the mutation is acquired in a marrow stem cell rather than inherited, it is present only in blood cells descended from that clone, which is also why a blood sample is the right specimen.

Most laboratories run the V617F screen first. If it comes back negative but the clinical picture still points strongly to PV, the next step is to sequence exon 12 of the gene, a different region where a smaller set of mutations can produce the same jammed-switch effect. Many labs now bundle this as a reflex: V617F first, exon 12 automatically if the first is negative.

MedlinePlus Genetics notes that JAK2 mutations are found in about 95 percent of people with PV, with exon 12 changes accounting for most of the rest. Turnaround time depends on the laboratory and on whether the exon 12 step is triggered; the hematologist’s office is the right place to ask when a particular result is expected.

What JAK2 mutation test results mean, including allele burden

A JAK2 mutation test result usually arrives in one of three forms, and each needs a different response.

A positive V617F result, in a person with a persistently raised hematocrit or hemoglobin and a low erythropoietin level, satisfies most of the WHO diagnostic criteria for PV. The 2016 WHO classification lists three major criteria: elevated hemoglobin or hematocrit, a bone marrow biopsy showing overgrowth of all three cell lines, and a JAK2 mutation. A low erythropoietin level is the minor criterion. Meeting all three major criteria, or the first and third major criteria plus the minor one, establishes the diagnosis.

A negative result does not close the door. It means the common mutation was not detected in that sample at that laboratory’s sensitivity. The clinician will weigh it against everything else and may order exon 12 sequencing, repeat the count, or proceed to a marrow biopsy.

Many reports also include a figure called the variant allele fraction or allele burden: the percentage of JAK2 gene copies in the sample that carry the mutation. A low fraction means the mutated clone makes up a small share of blood cells; a high fraction means it dominates. Research summarized by Mayo Clinic and others has linked higher allele burden with more pronounced overproduction and, in some studies, with higher rates of clotting or later progression. The honest position is that burden is informative but not yet a standalone decision tool. Clinicians use it as context, alongside age, prior clots and blood counts, rather than as a threshold that automatically triggers or withholds treatment.

One more scenario deserves a sentence. A JAK2 mutation occasionally turns up in someone with completely normal counts, a situation called clonal hematopoiesis. That is not PV, and it is not a diagnosis of anything by itself, though it does justify periodic monitoring with the clinician who ordered the test.

Can you have polycythemia vera and negative JAK2?

Yes, though it is uncommon, and the question is one of the most searched for good reason. Roughly 5 percent of people who meet every other criterion for PV test negative on the standard V617F screen, according to MedlinePlus Genetics. Most of that small group carry a mutation in exon 12 instead, which is why the reflex test exists. A very small remainder have neither detectable change and are described as JAK2-negative or, in older literature, triple-negative PV.

Several things can produce a negative result in someone who nonetheless has the disease. The allele burden may be below the detection limit of the assay used; sensitivity differs between laboratories and between older and newer methods. The sample may have been drawn after a phlebotomy or during an illness that temporarily shifted the mix of cells. Exon 12 may simply not have been tested. Any of these is a reason to repeat or extend testing rather than to abandon the diagnosis.

Equally, a negative test often means the red cell count is high for a secondary reason, and that is good news worth taking seriously. Secondary polycythemia is managed by addressing its cause: treating sleep apnea, stopping smoking, reviewing testosterone therapy, or investigating the kidneys. The clotting risk is generally lower than in PV, and the marrow is not harboring a clone.

When JAK2 is negative and the picture is still ambiguous, the bone marrow biopsy becomes decisive. Under the WHO criteria it is one of the three major criteria, and in a JAK2-negative person it is usually required. The sample is taken from the back of the hip under local anesthetic, and a pathologist looks for the characteristic overgrowth of red cell, white cell and platelet precursors with clustered, oversized platelet-forming cells. That pattern, plus a low erythropoietin level, can confirm PV even without a detectable mutation.

Polycythemia vera hematocrit levels: why 45 percent matters

Once PV is diagnosed, the hematocrit stops being a diagnostic clue and becomes the single most-watched treatment target. The reason is a trial rather than a tradition.

The CYTO-PV study, published in the New England Journal of Medicine and indexed on PubMed, randomly assigned 365 adults with PV to one of two strategies: keep the hematocrit below 45 percent, or allow it to sit between 45 and 50 percent. Over a median follow-up of about 31 months, the combined rate of death from cardiovascular causes or major thrombosis was 2.7 percent in the low-hematocrit group and 9.8 percent in the higher group. That is close to a fourfold difference, achieved with the same medicines used at different intensities.

Two points from that trial shape everyday practice. First, the 45 percent figure is a ceiling, not a cosmetic goal; the aim is to keep blood thin enough to flow freely, and clinicians will often individualize the exact number for women, whose baseline hematocrit tends to run lower. Second, the result applied to people who were already being treated; it does not suggest that anyone should attempt to manage their own count.

How the target is reached varies. Therapeutic phlebotomy, which removes a unit of blood much like a blood donation, lowers the hematocrit quickly and is often the first tool. Medicines that slow marrow production are added when phlebotomy alone is not enough or when other risk factors are present. Both are covered in the treatment section below.

A practical note for anyone reading their own results: the hematocrit drifts with hydration, time of day and recent illness. A reading of 46 on one draw and 44 on the next is not a treatment failure or a recovery. Trends over weeks, not single values, are what the care team acts on.

Polycythemia vera or secondary polycythemia? How the tests tell them apart

Most of the diagnostic work in the first weeks is about separating a marrow that is overproducing on its own from a marrow that is responding to a signal. The tests line up differently in each case, and a table makes the pattern easier to see than paragraphs do.

Finding	Typical in polycythemia vera	Typical in secondary polycythemia
Hematocrit and hemoglobin	Persistently raised	Raised, may fluctuate with the cause
White cells and platelets	Often raised as well	Usually normal
Erythropoietin level	Low or low-normal	Normal or high
JAK2 V617F or exon 12	Detected in about 95 percent	Not detected
Bone marrow biopsy	Overgrowth of all three cell lines	Red cell line expanded only, or normal
Spleen	May be enlarged	Usually normal size
Oxygen saturation	Normal	May be low, especially overnight

The erythropoietin level is the quiet hero of this table. In PV the marrow is running without instruction, so the kidneys sense plenty of oxygen and switch the hormone off; the level comes back low. In secondary polycythemia the kidneys are the ones shouting for more red cells, so the hormone is normal or high. A low level with a positive JAK2 test is close to definitive, which is why the WHO criteria list it as the minor criterion and why, when counts are very high, the biopsy can sometimes be waived: the 2016 WHO classification notes that marrow examination may not be needed when hemoglobin exceeds 18.5 g/dL in men or 16.5 g/dL in women, or hematocrit exceeds 55.5 or 49.5 percent respectively, alongside a JAK2 mutation and a low erythropoietin.

Secondary causes need their own workup, which may include overnight oxygen monitoring, a chest X-ray, kidney imaging and a careful medication review. Finding one does not rule out PV in every case, but it changes the odds considerably, and it often points to something that can be treated directly.

Who gets the JAK2 test now, and who is asked to wait and repeat?

Clinicians do not order the JAK2 test for every high hematocrit, and understanding why spares a lot of anxiety in the waiting room.

The test is usually ordered promptly when the hematocrit or hemoglobin is above the WHO thresholds on more than one occasion, when white cells or platelets are also raised, when the erythropoietin level is low, when the spleen is enlarged on examination, or when someone has already had an unexplained clot, particularly in an unusual site such as the veins of the liver or abdomen. In that last group the test is often sent even if the blood count looks normal, because a JAK2 mutation can precede the rise in hematocrit.

People are typically asked to wait and repeat when the first reading is only modestly raised, when there is an obvious secondary explanation that can be addressed first, or when the sample was clearly taken in a dehydrated state. A repeat count a few weeks later, after rehydration or a review of smoking or testosterone use, answers a lot of questions at no cost in time. NHS guidance on polycythaemia describes exactly this stepwise approach: confirm the count, look for a cause, then test for the mutation.

Waiting is not the same as dismissing. A good clinician will say why they are repeating rather than testing, what change in the numbers would move the decision, and when the next draw is due. If that explanation is missing, it is reasonable to ask for it.

A separate group is tested for reasons unrelated to red cells: people with a persistently high platelet count or unexplained marrow scarring, where the same mutation can underlie a different myeloproliferative neoplasm. A positive result in that setting still needs the full picture before anyone names the condition.

Is polycythemia vera hereditary?

In the vast majority of cases, no. The JAK2 mutation that drives PV is somatic, meaning it arises in a single blood-forming cell during a person’s lifetime and is not present in the egg or sperm. It cannot be passed to children, and a child of someone with PV does not need a JAK2 test on that basis alone. MedlinePlus Genetics describes PV as usually not inherited, with most cases occurring in people with no family history.

There is a small but real exception. Some families show more than one member with PV or a related myeloproliferative neoplasm, more often than chance would predict. Researchers believe inherited variation in or near the JAK2 gene can make a marrow cell slightly more likely to acquire the V617F change, nudging the odds upward without causing the disease directly. This is a predisposition, not a transmitted condition, and it is uncommon enough that routine screening of relatives is not recommended in current guidance.

What this means in practice: if a parent, sibling or child also has an unexplained high blood count, mention it, because it may change how closely a clinician looks. If relatives are healthy, there is no reason to test them, and no reason for them to worry. Genetic counseling is rarely needed for PV, but a hematologist can arrange it in the rare families where clustering is striking.

Why the mutation appears in the first place is still not fully understood. Age is the strongest association, consistent with the idea that DNA copying errors accumulate over decades. Exposure to high-dose radiation and certain industrial chemicals has been linked in some studies, but no single cause explains most cases, and nothing a person did or ate is responsible for acquiring it.

What the first weeks after diagnosis usually look like

The period between a positive JAK2 result and a settled routine is short by the standards of most chronic conditions, but it is dense with appointments, and knowing the shape of it helps.

The first hematology visit usually covers three things: confirming the diagnosis against the WHO criteria, placing the person in a risk category, and agreeing an initial plan. Risk is stratified mainly by two factors. Mayo Clinic and NHS resources both describe age over 60 and a history of a previous clot as the markers that move someone into the higher-risk group. Everyone else is considered lower risk, which changes the intensity of treatment rather than the goal.

If the hematocrit is well above target, phlebotomy often begins at or soon after that first visit. Each session removes roughly a unit of blood through a vein in the arm and takes a similar amount of time to a blood donation. Early on, sessions may be scheduled fairly close together until the count falls below the agreed ceiling; after that, the interval stretches out and is set by how quickly the count climbs back. The exact spacing is individual and belongs to the treating team.

Blood counts are repeated frequently in this phase, sometimes before each phlebotomy, and the hematologist will also check iron studies, because repeated blood removal gradually lowers iron stores. That is intentional, since low iron slows red cell production, so iron supplements are not usually started without specific advice.

Many people feel the viscosity symptoms ease within a few sessions: headaches lift, vision clears, the flush fades. Itching and fatigue can be slower to improve and are managed separately. By the end of the first couple of months most people have a predictable schedule, a target number they know by heart, and a sense of what their own counts do between visits.

How the results shape treatment choices

The two tests in the title do more than confirm a diagnosis; they set the direction of therapy. The hematocrit defines the target, and the JAK2 result, together with age and clot history, defines how aggressively to pursue it.

For lower-risk PV, the usual backbone is therapeutic phlebotomy to hold the hematocrit under the agreed ceiling, plus aspirin as prescribed by the clinician to reduce platelet stickiness. Mayo Clinic and NHS guidance describe this combination as standard, and the CYTO-PV trial supplies the evidence for the ceiling itself.

For higher-risk PV, or when phlebotomy alone cannot control the counts, a medicine that slows marrow output is added. Three classes are in mainstream use. Hydroxyurea, an oral agent that interferes with DNA synthesis in rapidly dividing cells, is the longest-established. Interferon alfa, given by injection, modulates the immune system and in studies has reduced the JAK2 allele burden in some people over time. JAK inhibitors such as ruxolitinib block the jammed signaling pathway directly and are typically reserved for people who do not tolerate or respond to the first option. Each has its own side-effect profile, monitoring requirements and typical timeline to effect, and the choice between them is made by the hematologist based on age, other conditions, pregnancy plans and how the blood counts respond.

Managing clot risk also means managing everything else that thickens blood or hardens arteries: blood pressure, cholesterol, diabetes, smoking, and prolonged immobility on long journeys. These are not footnotes; in a condition whose main danger is thrombosis, they can matter as much as the count.

None of this is a menu to choose from. It is a map of what a care team is weighing, offered so that the conversation in the consulting room makes more sense when it happens.

What people often get wrong about the JAK2 test

The same misunderstandings come up again and again in support forums, and correcting them early saves real distress.

The first is that a positive JAK2 test equals PV. It does not. The mutation also drives essential thrombocythemia and primary myelofibrosis, two related marrow conditions, and it can appear in people with normal counts as clonal hematopoiesis. The blood count, erythropoietin level and sometimes the marrow decide which, if any, condition is present.

The second is the mirror image: that a negative test rules PV out. As discussed above, about 5 percent of cases are V617F-negative, most of them carrying exon 12 mutations instead, and a very few have no detectable mutation at all.

Third, people often assume the allele burden is a severity score, with a higher percentage meaning a worse disease. Burden correlates with some outcomes in research, but it is one input among several, and clinicians do not escalate treatment on that number alone.

Fourth, there is a widespread belief that PV is inherited and that children should be tested. For nearly everyone the mutation is acquired, not passed on, and routine family screening is not recommended.

Fifth, some assume donating blood is the same as therapeutic phlebotomy and can replace it. Blood donation services generally do not accept donors with a diagnosed blood cancer, and phlebotomy for PV is scheduled to a target, not to a calendar.

Finally, the word cancer trips people into imagining a short timeline. PV is a chronic condition. Mayo Clinic describes it as a slowly progressing disease that many people live with for decades under treatment, and the main medical goal is preventing clots rather than eradicating the clone. Understanding that reframes almost everything that follows the diagnosis.

Questions to ask your care team

A hematology appointment goes faster than most people expect, and the questions that matter tend to arrive in the car park afterward. Bringing a short list in writing changes that. These are the ones that experienced patients say they wish they had asked at the start.

• Which of the WHO criteria do my results meet, and is anything still missing before the diagnosis is considered confirmed?
• Was exon 12 tested, or only V617F, and what allele burden was reported?
• Do I need a bone marrow biopsy, and if not, why has it been waived in my case?
• What is my personal hematocrit target, and how often will it be checked?
• Which risk category am I in, and what would move me into a different one?
• What is the plan if phlebotomy alone does not hold the count, and what would prompt adding a medicine?
• Which symptoms should I treat as urgent, and whom do I call out of hours?
• How will iron levels be monitored, and should I avoid iron supplements or iron-rich foods?
• Is there anything about my other medicines, including hormone therapy or over-the-counter products, that interacts with this condition?
• How will we know over the years whether the disease is progressing, and what would that look like on my results?

Two habits make the answers more useful. Ask for a copy of each blood count and keep the hematocrit and platelet trends in one place; a simple chart on a phone is enough. And ask the team to explain any change in plan in terms of the numbers that drove it. People who understand why their phlebotomy interval shortened or lengthened tend to feel far steadier between visits than those who are simply told a date.

When to call your doctor

PV is managed in the clinic, but its most serious complications happen at home, often without warning. Knowing which symptoms cannot wait is part of the treatment plan, not an addition to it.

Call emergency services immediately for sudden weakness or numbness on one side of the body, slurred speech, a drooping face, sudden loss or blurring of vision in one eye, a sudden severe headache unlike any before, chest pain or pressure, or breathlessness that comes on abruptly. These can signal a clot in the brain, heart or lungs, and minutes matter.

Contact the hematology team or an urgent care service the same day for a swollen, painful or warm calf; severe or persistent abdominal pain, especially in the upper right side, which can indicate a clot in the veins of the liver; vomiting blood or passing black stools; unusual bruising or bleeding that does not stop; or a fever that does not settle, particularly if taking a medicine that lowers blood counts.

Burning pain or redness in the hands or feet, worsening itching, or a feeling of fullness under the left ribs are less urgent but should be reported at the next contact, because they can reflect a count that has drifted above target or a spleen that is enlarging.

Before any surgery, dental extraction or long-haul flight, let the team know in advance. Immobility and surgery both raise clot risk, and the plan may need adjusting beforehand rather than afterward.

If in doubt, call. Hematology teams would far rather hear about a false alarm than learn about a missed clot, and every decision about what to do next sits with them.

Frequently asked questions

Can you have polycythemia vera and negative JAK2?

Yes, but rarely. About 5 percent of people who meet the other criteria test negative on the standard V617F screen, and most of those carry a mutation in exon 12 of the JAK2 gene instead. A small remainder have no detectable mutation at all. When the first test is negative but the picture still fits, clinicians add exon 12 sequencing and usually a bone marrow biopsy before deciding.

What is polycythemia vera?

Polycythemia vera is a chronic myeloproliferative neoplasm in which a mutated marrow stem cell produces too many red blood cells, and often too many white cells and platelets. The excess cells thicken the blood and raise the risk of clots. It is classified as a slow-growing blood cancer, is usually diagnosed around age 60, and is managed over many years rather than treated in a single course.

Which blood test shows polycythemia?

A routine complete blood count is where polycythemia first shows up, through a raised hematocrit and hemoglobin. Those numbers signal that red cells are too concentrated but do not say why. An erythropoietin level, a JAK2 mutation test and sometimes a bone marrow biopsy are then used to distinguish polycythemia vera from secondary causes such as sleep apnea, smoking, lung disease or hormone therapy.

Can polycythemia vera be hereditary?

Usually not. The JAK2 mutation behind most cases is acquired in a single blood-forming cell during life and is not passed to children. A small number of families show clustering of PV or related conditions, which researchers attribute to inherited variation that slightly raises the chance of acquiring the mutation. Routine testing of healthy relatives is not recommended, though a family history is worth mentioning.

What do jak2 mutation test results look like on a report?

A report typically states whether the V617F mutation was detected, whether exon 12 was tested, and often a variant allele fraction, the percentage of JAK2 gene copies carrying the change. Detected with a raised hematocrit and low erythropoietin supports a PV diagnosis. Not detected means the mutation was not found at that laboratory’s sensitivity; the clinician decides whether to extend testing.

What are typical polycythemia vera hematocrit levels at diagnosis and during treatment?

At diagnosis the hematocrit is above the WHO thresholds of 49 percent in men or 48 percent in women, and sometimes well above. During treatment the aim, based on the CYTO-PV trial, is to keep it below 45 percent, with individual targets set by the hematologist. Single readings drift with hydration and illness, so the care team acts on trends over weeks rather than one value.

Does a jak2 negative polycythemia vera diagnosis mean milder disease?

Not necessarily. JAK2-negative PV, including exon 12 cases, is managed with the same goals of hematocrit control and clot prevention. Some studies suggest exon 12 cases present with a more isolated rise in red cells and fewer platelet or white cell changes, but the clotting risk is still real. Risk category is set by age and prior clots, not by which mutation is present.

Is polycythemia vera hereditary if a parent had it?

Having a parent with PV raises the chance only slightly, and most children of affected parents never develop it. The mutation itself is not inherited. Current guidance does not recommend screening relatives who have normal blood counts and no symptoms. If a relative has an unexplained high count or an unusual clot, that should be investigated on its own merits with a clinician.

Does a positive JAK2 test in a healthy person mean they have cancer?

No. A JAK2 mutation can be present in people with normal blood counts, a state called clonal hematopoiesis, which is not polycythemia vera or any other diagnosis by itself. It does mean the clone is there, so the clinician who ordered the test will usually suggest periodic blood counts to watch for change. Treatment is not started on a mutation alone.

Why is erythropoietin measured alongside the JAK2 test?

Erythropoietin is the kidney hormone that instructs the marrow to make red cells. In PV the marrow overproduces on its own, so the kidneys switch the hormone off and the level is low. In secondary polycythemia the kidneys are driving production and the level is normal or high. A low level with a positive JAK2 test is one of the strongest confirmations of PV available.

References

• MedlinePlus Genetics: Polycythemia vera
• NHS: Polycythaemia

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.