Why blossom end rot is not a calcium deficiency: understanding apical necrosis.

Why blossom end rot is not a calcium deficiency: understanding apical necrosis

Example of a tomato showing apical necrosis, also known as "blossom end rot" (brown necrotic spot at the end of the fruit).

The apical necrosis, commonly referred to asblossom end rotin tomatoes, is a common physiological disorder that manifests as a dark, sunken spot at the bottom of the fruit. Unlike a disease, it is a disorder related to growing conditions and the physiology of the plant. Varieties with large or elongated fruits (e.g. San Marzano, Beefsteak) are particularly sensitive to it. This phenomenon is especially observed in hot and dry weather during the summer, and can affect a significant portion of the crop if no measures are taken.

Causes of "blossom end rot" (apical necrosis)

Apical necrosis results from a localized deficiency ofcalciumin the fruit tissues, causing cellular collapse and the death of cells at the end of the fruit. It is important to note that this deficiency is generally not due to a lack of calcium in the soil, but rather to poor absorption and distribution of this element within the plant. Indeed, even if the plant contains sufficient calcium, various factors can prevent this element from reaching the developing fruits. Recent research confirms that the underlying causes of "blossom end rot" are related to a disruption of calcium homeostasis in the plant, combined with irregular watering conditions.

Several environmental factors contribute to this calcium imbalance. The occurrence of "blossom end rot" is thus favored by various abiotic stresses: soil that dries out between waterings, an atmosphere that is too humid (or conversely, very dry air), and high temperatures disrupt the transport of calcium within the plant. For example, a water deficit in the soil reduces the absorption of Ca by the roots, while high evapotranspiration during hot and dry weather preferentially directs calcium to the leaves at the expense of the fruits.

The physiology of the plant also plays a role. Large fruits that grow very quickly (due to the variety or excessive nitrogen fertilization) have an increased risk of apical necrosis, as the faster the fruit grows, the more the calcium content of its tissues dilutes if root absorption does not keep up.

Technical passage

(For those who do not want as much detail, feel free to skip to the next chapter)

Understanding in depth the causes of apical necrosis ("blossom end rot") in tomatoes

1. The central role of calcium in the structure of fruit tissues

Calcium (Ca²⁺) is an element essential for the cohesion and stability of cellular membranes. In the fruit, it is indispensable at several levels:

✔ Cohesion of the walls via pectin

Ca²⁺ binds to the polygalacturonic acids of pectin to formionic bridges(the "egg-box" model described by Grant et al., 1973).

→ Without calcium, the wall loses its rigidity, the cells break, and a necrotic area appears.

✔ Stability of plasma membranes

A calcium deficiency increases the membrane permeability, causing ion leakage and oxidative stress.

→ This leads to the collapse of the tissue at the apical level.

✔ Immobility of calcium

Calcium is not very mobile in the phloem.

→ Once incorporated into the leaves, it can hardly be redistributed to the fruits.

This point is essential to understand why foliar sprays are ineffective: calcium applied to the leaves does not migrate to the fruits.

2. Why does the fruit locally lack calcium?

The soil may contain a lot of calcium, but the flow of calcium to the fruitdepends entirely on the water absorbed by the roots and transpired by the plant..

✔ Calcium circulates almost exclusively in the xylem.

The fruit, especially during rapid growth, receives less xylem flow than a leaf.

Young fruits are initially well irrigated by the xylem, but as soon as the phloem takes over as the main channel (sugar accumulation phase), the supply of calcium decreases significantly..

→ If there is water stress at the wrong time (10–20 days after fruit set), the transport of calcium drops sharply.

✔ Physiological priority to the leaves

During high heat, leaf evapotranspiration skyrockets.

Calcium follows the dominant transpiration flow →it is directed towards the leaves, not towards the fruits.

The fruits then receive insufficient amounts.

✔ Calcium dilution in fast-growing fruits

Very rapid growth — favored by:

• excess ammoniacal nitrogen,
• heavy irrigation after water stress,
• large-fruited varieties —
  causes a dilution of calcium in the fruit tissues.

3. Water stress: the most determining factor

✔ Alternation of drought / excess water

This is the main trigger observed in the agronomic literature (Taylor & Locascio, 2004).

• Drought → cessation of Ca absorption.
• Abrupt resumption of irrigation → cellular growth resumes faster than calcium supply.
  → The apical zone, the farthest from the peduncle, becomes deficient.

✔ Soils that are too dry, poorly buffered or poorly structured

Sandy soils, low in organic matter, or covered with too thin a mulch:

→ abrupt fluctuations in water content → fluctuations in Ca flow.

✔ Ionic competition in the soil

Ca²⁺ can be blockedby excess of:

• K⁺ (potassium),
• NH₄⁺ (ammonium),
• Na⁺ (sodium).

These ions compete at the root absorption sites.(evidence demonstrated by Saure, 2014).

→ Even with 2000–3000 mg/kg of Ca in the soil, the plant can be functionally deficient.

4. Role of climate: high temperatures and humidity of the air

✔ High temperatures (> 30–32°C)

• Increase transpiration
• Promote rapid fruit growth
• Reduce the hydraulic conductivity of the xylem

→ All of this exacerbates the lack of Ca in the apical zone.

✔ Air humidity too low

RH < 50 % → very high leaf transpiration →priority of water flow to the leaves.

✔ Air humidity too high in the greenhouse

RH > 85 % → low transpiration → xylem flow slows down →calcium transport significantly reduced.

→ The paradox: theblack bottomcan appear in overly humid conditions.

5. Role of soil and microbiology

✔ Soil structure

Roots lacking oxygen (suffocating, too heavy soils) → reduced root absorption.

✔ Mycorrhizae

Some publications (Al-Karaki, 2013) show that mycorrhizal plants absorb Ca and Mg better.

→ Soils poor in biological activity therefore increase the risk indirectly.

✔ Soil pH

• pH < 5.5 → Ca becomes less available.
• Optimal pH for tomato: 6.3 – 6.8.

6. Varietal and genetic factors

The at-risk varieties are those:

• with elongated fruits (San Marzano),
• very large fruits (Beefsteak),
• rapid growth,
• thin cuticle.

They have a less homogeneous internal distribution of calcium than small round varieties.

In summary (very technical version)

Apical necrosis results from a combination of factors that cause:

1. A reduction in Ca flow in the xylem (water stress, humidity, heat, salinity).
2. An ionic competition at the root level (excess K⁺, NH₄⁺).
3. A priority allocation of Ca to the leaves (high transpiration).
4. A dilution of Ca in the fruit(rapid growth).
5. The immobility of Ca in the phloem, preventing any subsequent correction.
6. A weakening of the membranes and pectin, leading to apical tissue death.

Phew... end of the technical chapter!

Prevention and solutions to avoid apical necrosis

Although a fruit affected by apical necrosis is irrecoverable, one can prevent this disorder on subsequent fruits by improving growing conditions. Here are the main measures to implement to avoid the "black bottom" of tomatoes:

• Regular watering and moist soil.: Maintain soil moisture as consistently as possible, without alternating between drought and excess water. Frequent watering that is appropriate for the climate is essential; never let the soil dry out completely, especially during high heat. During heat waves, it may be necessary to water twice a day rather than once in large quantities. Using mulch at the base of the plants is also recommended to keep the soil cool and limit evaporation. Finally, ensure that irrigation reaches the entire root zone to encourage deep rooting, as only the active tips of the roots absorb calcium.
• Balanced nutrition and growth: Avoid excessive applications of fertilizers rich in ammonium nitrogen (NH4+) or potash (K) that can compete with calcium absorption. Favor moderate applications and, if possible, nitrate-based fertilizers (NO3-) rather than ammonium, as nitrate promotes the availability of calcium for the plant. Also, ensure that the soil pH is around neutrality (6.5), as overly acidic soil (pH < 6) reduces calcium availability. Also moderate the vigor of your plants: too rapid and lush growth tends to worsen the calcium imbalance. Avoid nitrogen over-fertilization, and do not hesitate to remove some fruits or leaves from very vigorous plants to balance their development. Finally, note that calcium sprays on foliage are generally ineffective, as calcium does not move well from leaves to fruits.
• Climate control (in greenhouse): In protected cultivation, control humidity and temperature to maintain optimal transpiration. During high heat, provide shading (covers, whitewashing of glass) or misting to prevent excessive transpiration of the plants. Conversely, in cool and very humid weather, ventilate and moderately heat the air to reduce ambient humidity: this will increase sap flow and thus the supply of calcium to the fruits.

In summary, tomato blossom end rot is primarily a management issue of water and nutritional balance, which hinders the transport of calcium to the fruits. By maintaining regular soil moisture, appropriate fertilization, and controlled growth of the plants, the risk of "blossom end rot" in tomatoes can be significantly reduced.

Grafting: an indirect protection against blossom end rot

Grafting is often presented as a "magic solution" to many tomato cultivation problems. Regarding the blossom end rot (black bottom), it is important to be precise: grafting does not directly protect against this physiological disorder. The primary cause of black bottom remains a failure in calcium supply to the fruits, related to sap flow and water conditions, not a simple root defect that grafting would "correct" instantly. Grafting does not directly protect against this physiological disorder. The primary cause of black heart remains a failure to supply calcium to the fruits, related to sap flow and water conditions, not a simple root defect that grafting would "instantly correct."

On the other hand, grafting can play an indirect but real role in reducing the risk. The rootstocks selected for tomatoes indeed present:a dans la réduction du risque. Les porte-greffes sélectionnés pour la tomate présentent en effet :

• un more powerful and deeper root system,
• a superior water absorption capacity,
• a better stress tolerance(drought, heat, salinity),
• a more efficient functional continuity of the xylem. plus efficace.

These characteristics allow for a more regular hydromineral supply, leading to a more stable flow of calcium in the plant. This does not guarantee the absence of blossom end rot — as irregular watering, unbalanced fertilization, or excessive transpiration can still disrupt calcium distribution — but it reduces the sensitivity of the plant to environmental fluctuations.

Grafting is not a direct solution to blossom end rot, but by improving root vigor, water supply stability, and the overall resilience of the plant, it makes the tomato less vulnerable to conditions that trigger apical necrosis.

The “miracle recipes” against blossom end rot: why they don’t work

Disclaimer

“That Uncle Gérard, in the Jura, religiously buries egg shells and has never seen blossom end rot does not demonstrate the effectiveness of the recipe; it mainly shows that his tomatoes were doing very well despite the shells, not because of them.”

Apical necrosis generates many popular “tips,” often well-intentioned, but none actually act on the physiological mechanism responsible.: the transport of calcium in the xylem to the fruit.

Here is a rigorous, point-by-point analysis of the most common techniques — and the reasons why they fail.

1. Eggshells

🔧 Assumed principle

Burial of crushed eggshells in the soil to “provide calcium.”

❌ Why this doesn't work

Eggshells are composed of calcium carbonate (CaCO₃)in a very stable crystalline form.

→ They take several years to decompose, sometimes more than 2–3 years depending on the soil pH and its biological activity.

Even when finely crushed, their solubilization is extremely slow, much slower than the growth cycle of a tomato. The calcium produced arrives too late and does not affect the xylem flow, which is the real cause of blossom end rot.

They may be useful for correcting acidity in the long term, but they neither cure nor prevent blossom end rot in the short term.

“The successes attributed to eggshells often stem from a confusion between correlation and causation — a very common bias, even among the most convinced gardeners.”

2. Diluted milk (foliar sprays or watering)

🔧 Assumed principle

Milk would contain assimilable calcium; sprayed on the foliage or poured at the base, it would “nourish” the fruits.

❌ Why this doesn't work

1. Calcium does not migrate from the foliage to the fruits.
   Ca is immobile in the phloem. A leaf sprayed with milk can absorb a little Ca… but nothing will happen to the fruit..
2. The calcium from milk does not enter the plant easily.
   Dairy Ca is mostly bound to casein,which is not soluble in bioavailable ions.

3. The risks increase. :

   • Milk fermentation → fungal and bacterial development.
   • 
     

Conclusion: Milk has no physiological effectiveness on calcium transport to the fruit.

3. Do not water the tomatoes ("you should never water")

🔧 Assumed principle

Lack of watering makes tomatoes "stronger" and would prevent blossom end rot.

❌ Why this doesn't work

It isthe exact oppositeof the physiology of blossom end rot.

Calcium reaches the fruits only through the flow of water in the xylem..

→ If we reduce watering:

• root absorption drops,
• transpiration decreases,
• Ca transport decreases,
• the apical zone of the fruit becomes deficient.

Worse yet:

Alternating drought → sudden rehydration is the number one trigger for blossom end rot.

4. Seaweed powders, lithothamnion or liquid seaweeds

🔧 Assumed principle

Seaweeds contain calcium and trace elements, thus they "balance" the plant.

❌ Why this doesn't work

Lithothamnion or seaweed extracts can:

• slightly increase the pH,
• enrich the soil with minerals,

but the calcium provided does not address the real problem :

→ a distribution issue, no availability.

As with other calcium inputs, if the water conditions are poor, the Ca still does not reach the fruit.

Moreover, the massive use of lithothamnion poses ecological problems (destructive extraction of marine habitats).

5. Wood ash

🔧 Assumed principle

Ash contains potassium and calcium, it "strengthens" the plants.

❌ Why this doesn't work

Ash is rich in potassium (K): 10–30%.

And K is antagonistic to Ca at root absorption sites.

→ Adding ash often worsens apical necrosis by:

• reducing the absorption of Ca²⁺ (K+/Ca2+ competition),
• increasing soil salinity,
• disrupting root osmosis.

Thus, ash does not no beneficial action on blossom end rot, and may even increase its frequency.

6. Spraying pure calcium (calcium nitrate, chelates, etc.)

🔧 Assumed principle

Spraying calcium on fruits corrects the deficiency.

❌ Why this doesn't work

• Calcium only penetrates the skin of the fruit marginally.
• And even if it did, the necrotic area is located inside, in the sub-epidermal tissues.
• Calcium sprayed on leaves never reaches the fruit (phloem immobility).

Sprays may slightly reduce the severity if applied very early, but never prevent an episode related to watering or temperatures.

To summarize simply:"Relying on a calcium spray to correct blossom end rot is about as effective as hoping to rejuvenate a 90-year-old with anti-wrinkle cream: the intervention is superficial, late, and completely disconnected from the actual mechanism of the problem."

7. Adding vinegar, yogurt, coffee grounds, or other acids "to release calcium"

🔧 Assumed principle

Acidity would solubilize calcium from the soil.

❌ Why this doesn't work

These additions essentially modify:

• the local pH (often too strongly),
• the soil microbiology.

They do not increasetheentry speed of Ca²⁺ into the xylem andhave no effect on the fruits in growth.

Conclusion: the problem is never the lack of calcium in the soil

In 95% of scientifically measured cases, soils affected by “blossom end rot” contain already much more calcium than necessary.

The only real problem is:

A deficiency in the transport of calcium to the fruit, due to irregularities in watering, temperature, or ionic balance.

No miracle recipe can fix this.

The only truly effective measures are:

• regular watering and never alternating,
• control of vigor,
• balanced fertilization (not too much K or NH₄⁺),
• homogeneous climate in the greenhouse,
• living soil
• suitable varieties.

Ranking of elongated varieties least sensitive to blossom end rot

Ranking (not exhaustive) of varieties from most sensitive to least sensitive to blossom end rot)

1. 
   
2. Tulip yellow(andgreen Tulip): One of the most sensitive tomatoes to blossom end rot
3. Buratino
4. San Marzano
5. Lucky tiger(it's more of an "olive tomato" than a "horn tomato", but it remains sensitive to blossom end rot)
6. Roma (resistance "medium, but taste also very average)
7. Cuban pepper like(average resistance, but unique taste!)
8. Boxer rebellion CTR(good resistance)
9. Blush
10. Tulip(very good resistance)
11. Smiley worms
12. Yellow fire(the best compromise "taste/resistance")
13. Ukrainian Sabre(one of the horned varieties least sensitive to blossom end rot)

Sources

• bioactualites.chbioactualites.chbioactualites.chSamuel Hauenstein,Apical necroses on tomatoes and peppers(FiBL, 2020) – Detailed technical article explaining the causes (localized calcium deficiency, climatic factors) and proposing preventive measures in market gardening.
• popups.uliege.bepopups.uliege.beTh. R'him & H. Jebari (2008),Apical necrosis in relation to certain parameters... in chili– Scientific study showing that a local deficiency in Ca in the fruit, combined with factors such as humidity (air/soil) and temperature, leads to the development of BER (apical necrosis).
• pubmed.ncbi.nlm.nih.govY. Topcu et al. (2022),Blossom-end rot: a century-old problem in tomato– Scientific review confirming that BER is associated with a disruption of calcium homeostasis and irregular watering.
• A cellular hypothesis for the induction ofblossom-end rotintomatofruitLC Ho,PJ White- Annals of Botany, 2005 - academic.oup.com… • Background The incidence ofblossom-end rot(BER) is generally associated with a calcium (Ca) deficiency in the distal portion oftomatofruits.